16.3: Immediate Hypersensitivities: Type III - Biology

16.3: Immediate Hypersensitivities: Type III - Biology

We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

Learning Objectives

  1. Describe the mechanism for Type III (immune complex-mediated) hypersensitivity and give 2 examples.

Mechanism: This is caused when soluble antigen-antibody (IgG or IgM) complexes, which are normally removed by macrophages in the spleen and liver, form in large amounts and overwhelm the body (see Figure (PageIndex{1})). These small complexes lodge in the capillaries, pass between the endothelial cells of blood vessels - especially those in the skin, joints, and kidneys - and become trapped on the surrounding basement membrane beneath these cells (see Figure (PageIndex{2})). The antigen/antibody complexes then activate the classical complement pathway (see Figure (PageIndex{3})). This may cause:

a. Massive inflammation, due to complement protein C5a triggering mast cells to release inflammatory mediators;

b. Influx of neutrophils, due to complement protein C5a, resulting in neutrophils discharging their lysosomes and causing tissue destruction through extracellular killing and causing further inflammation (see Figure (PageIndex{4}) and Figure (PageIndex{5}));

c. MAC lysis of surrounding tissue cells, due to the membrane attack complex, C5b6789n;

d. Aggregation of platelets, resulting in more inflammation and the formation of microthrombi that block capillaries; and

e. Activation of macrophages, resulting in production of inflammatory cytokines and extracellular killing causing tissue destruction.

This can lead to tissue death and hemorrhage.

Examples include:

  • serum sickness, a combination type I and type III hypersensitivity;
  • autoimmune acute glomerulonephritis;
  • rheumatoid arthritis;
  • systemic lupus erythematosus;
  • some cases of chronic viral hepatitis; and
  • the skin lesions of syphilis and leprosy.


  1. Type III (immune complex-mediated) hypersensitivity is caused when soluble antigen-antibody (IgG or IgM) complexes, which are normally removed by macrophages in the spleen and liver, form in large amounts and overwhelm the body.
  2. These small complexes lodge in the capillaries, pass between the endothelial cells of blood vessels - especially those in the skin, joints, and kidneys - and become trapped on the surrounding basement membrane beneath these cells.
  3. The antigen/antibody complexes then trigger excessive activation of the classical complement pathway leading to a massive inflammatory response, influx of neutrophils with extracellular killing of body tissue, MAC lysis of tissue, and aggregation of platelets and macrophages.
  4. Examples include Serum sickness, autoimmune acute glomerulonephritis, rheumatoid arthritis, and systemic lupus erythematosus.


Study the material in this section and then write out the answers to these questions. Do not just click on the answers and write them out. This will not test your understanding of this tutorial.

  1. Describe the mechanism for Type III (immune complex-mediated) hypersensitivity and give 2 examples. (ans)

Quick Notes on Hypersensitivity (With Diagram)

Immune response recruits and mobilizes a series of effector molecules that induce a localized inflammatory response, which ultimately removes the antigen.

This inflammatory response usually does not extensively damage the host tissues. But under certain conditions, the inflammatory response produces deleterious effects, resulting in significant tissue damage or even death this is termed as hypersensitivity or allergy.

Hypersensitive reactions may develop in the course of either humoral or cell-mediated immune responses. The phenomenon of hypersensitivity was discovered during the early 19th century by two French scientists. Porter and Richet, who concluded that toxin from a kind of jelly fish induced ‘overreaction’ in dogs they termed this overreaction as anaphylaxis, which is a type (Type III) of hypersensitivity.

Hypersensitivity has been classified into the following four types by Gell and Coombs:

(i) IgE-mediated (Type I) hypersensitivity,

(ii) Antibody-mediated cytotoxic (Type II) hypersensitivity,

(iii) Immune-complex- mediated (Type III) hypersensitivity, and

(iv) Delayed-type (Type IV) hypersensitivity (DTH).

The first three types of hypersensitivities are grouped together as immediate hypersensitivity since the symptoms become manifest within minutes or hours after a sensitized recipient encounters the antigen. The DTH, on the other hand, is so called because symptoms develop days after the exposure to the antigen. The features of the four types of hypersensitive responses are summarised in Table 43.1.

4 Main Types of Hypersensitivity | Immunology

Several types of hypersensitive reactions can be identified, reflecting differences in the effector molecules generated in the course of the reaction. Gell and Coomb described four types of hyper­sensitivity reactions (Types I, II, III and IV). The first three types are antibody-mediated and the fourth type is mediated mainly by T-cell and macro-phases i.e. cell-mediated (Table 11.1 and 11.2 Fig. 11.2).

1. Type I Hypersensitivity:

Type I hypersensitive reactions are the com­monest type among all types which is mainly induced by certain type of antigens i.e. allergens. Actually anaphylaxis means “opposite of protec­tion” and is mediated by IgE antibodies through interaction with an allergen.

During the activity, this class of antibody (IgE) binds with high affinity to FC (Fragment crystalized) receptors on the surface of constant domains of tissue mast cells and blood basophils. Such IgE-coated mast cells and basophils are said to be sensitized. When the indi­vidual is exposed to the same allergen again, then it cross-links the membrane bound IgE on sensi­tized mast cells and basophils and degranulation of those cells result (Fig. 11.3).

(ii) Biological effects:

1. Normally anaphylactic responses are of a mild type producing symptoms— like hay-fever, running nose, skin erup­tions called as ‘nives’ or breathing diffi­culties.

2. The pharmacologically active mediators released from the granules exert biological effects on the surrounding tissues.

3. In some cases, the responses may be severe, develop within a few minutes (2-30 mins) and may even cause death before any medical help is called anaphylactic shock.

4. The principal effects of vasodilation and smooth muscle contraction may be either systematic or localized.

(iii) Components of type-I reactions:

There are different types of components which are required for type-1 reactions:

3. Mast cells and basophils

4. IgE—binding FC receptors.

5. High—affinity and low-affinity receptors.

(iv) Therapy for Type-I hypersensitivity:

1. The first step in controlling type I is to identify the offending allergen and avoid contact if possible.

2. Removal of house pets, dust-control mea­sures.

3. Repeated injections of increasing doses of allergens called hypo sensitization.

4. Enhancement of phagocytosis by IgG antibody which is referred to a blocking antibody because it competes for the aller­gens, binds and forms a complex that can be removed by phagocytosis.

5. Successful use of anti-histamine drugs result better with respect to type I hyper­sensitivity.

2. Type II Hypersensitivity:

Type II hypersensitive reactions are those in which tissue or cell damage is the direct result of the actions of antibody and complement.

This type of reaction is resulted by blood- transfusion reactions in which host antibodies react with foreign antigens present on the incompatible transfused blood cells and mediate destruction of these cells.

Antibody can mediate cell destruction by activating the complement system to create pores in the membrane of the foreign cell by forming membrane attack complex (MAC). This can also be mediated by antibody dependent cell-mediated cytotoxicity (ADCC).

A faulty cross-matching leads to haemolysis of the donor’s erythrocytes in the blood vessels of the recipient due to the alloantigen of the donor’s erythrocytes react with the antibodies in the serum of the recipient and in combination with activated complement, the erythrocytes undergo haemolysis (Fig. 11.4).

1. Haemolytic disease of the newborn deve­lops when maternal IgG antibodies speci­fic for foetal blood-group antigens cross the placenta and destroy foetal red blood cells. Severe haemolytic disease of the new born is called erythroblastosis foetalis, when an Rh + foetus expresses an Rh antigen on its blood cells that the Rh – mother does not express it (Fig. 11.5).

2. Certain antibiotics (e.g. penicillin, cephalo­sporin and streptomycin) can absorb non- specifically to proteins on RBC mem­branes, forming a complex similar to a hapten-carrier complex and gradually induces anaemia called drug-induced haemolytic anaemia.

3. Type III Hypersensitivity:

When an antigen enters within the body then the antibody reacts with antigen and generates immune complex. This immune complex gradu­ally facilitates removal of antigen by phagocytic activity of body. Large amount of immune com­plexes lead to tissue-damaging Type III hype­rsensitivity. For this reason Type III is called immune complex hypersensitivity.

1. These reactions develop when immune complexes activate the complement sys­tem’s array of immune effector molecules. Complement components (C3a, C4a, C5a) split and produce anaphylatoxins which cause localized mast cell degranulation and increase local vascular permeability.

2. When formed bulky antigen-antibody com­plexes aggregate and combine with the acti­vated complement, they chemotactically attract the polymorphonuclear leucocytes. These cells release lysosomal enzymes in large quantities to cause tissue damage.

1. The recipient of a foreign antiserum deve­lops antibodies, specific for the foreign serum proteins from circulating immune complexes and within days or weeks after exposure to foreign serum antigens, an individual starts to develop serum sick­ness including fever, weakness, vasculitis (rashes) with edema, erythema, lymphadenopathy, arthritis and glomerulo­nephritis.

2. Due to deposition of IgG antigen comple­xes in the blood vessels cause local damage and deposit in blood vessels of kidney glomeruli called Arthus Reaction.

3. Inhalation of bacteria and fungal spores gives rise to a disease called farmer’s lung forming immune complexes in the epithe­lial layers of the respiratory tract.

4. Another type of hypersensitive reaction is known as lupus i.e. systemic lupus erythematosus. It is produced as a result of inter­action of IgG and the nucleoproteins of the disintegrated leucocytes (auto-antigens). Lupus is an autoimmune disease.

4. Type IV Hypersensitivity:

Type IV hypersensitivity is the only type of delayed hypersensitivity. It is mainly controlled by T-cells, macrophages and dendritic cells. It is not the instant response but it is manifested after the second exposure to an allergen. The appea­rance of allergic symptoms come in delay.

Delayed hypersensitivity is maintained by T- lymphocytes. T-cells (lymphocytes) have two main types—the CD4 + cells and CD8 + cells. Type IV hypersensitivity requires CD4 + type. The spe­cial group of CD4 + cells take part in type IV hyper­sensitivity and are called T-D cells (delayed). Again T-helper cell (TH cell) includes T-D cells which constitutes the bulk of CD4 + T-cells. TH cells are again distinguished into TH-1 and TH-2 type, of which TH.2 cells are mainly responsible for acti­vation of B-cell to produce immunoglobulins and TH-1 cells are involved in causing the inflamma­tory responses including delayed hypersensitivity reactions (Fig. 11.6).

1. A microbial agent that elicits a delayed hypersensitivity is tuberculin which is a purified protein derivative (PPD) of tubercle bacilli (Mycobacterium tuberculo­sis). Mycobacterium leprae, the microbial agents also stimulate delayed hyper­sensitivity.

2. The tuberculin skin test (Mantoux test) is used to determine if a person has T-cell mediated reactivity towards tubercle bacilli (also known as Koch’s bacilli).


Type II hypersensitivity is also known as cytotoxic hypersensitivity or antibody-mediated hypersensitivity reactions. Also, it may affect a variety of organs and tissues. Type II hypersensitivity reactions involve antibody-mediated destruction of cells by immunoglobulins of heavy chain classes other than IgE.

Antibody bound to a cell-surface antigen can induce death of the antibody-bound cell by three distinct mechanisms.

  • First, the antibody bound to a cell surface can activate the complement system, creating pores in the membrane of a foreign cell.
  • Secondly, antibodies can mediate cell destruction by the antibody-dependent cell-mediated cytotoxicity (ADCC). In this process, cytotoxic cells with Fc receptors bind to the Fc region of antibodies on target cells and promote killing of the cells.
  • Finally, the antibody bound to a foreign cell also serve as an opsonin, enabling phagocytic cells with Fc or C3b receptors to bind and phagocytose the antibody-coated cell


  • Blood transfusion/transfusion reactions: When transfusion with mismatch blood occurs, a transfusion reaction takes place due to the destruction of the donor RBCs through the iso-hemagglutinins against the foreign antigen.
  • Erythroblastosis Fetalis: it develops when maternal antibodies specific for fetal blood group antigens cross the placenta and destroy fetal RBCs. As a result, severe hemolysis occurs, leading to anaemia and hyperbilirubinemia, which can even be fatal.
  • Drug-Induced Hemolysis: Certain drugs (such as penicillin, quinidine, phenacetin, etc.) may induce hemolysis of red blood cells. They attach to the surface of red blood cells and induce the formation of IgG antibodies. These autoantibodies then react with red blood cell surface, causing hemolysis.

S ymptoms

Redness and swelling are major symptoms under this categories. Generally, it develops from any where between minutes to hours.


The treatment includes anti-inflammatory and immunosuppressive agents.


A negative reaction to wireless signals. Also called "gadget allergies," symptoms can be headaches, nausea, ringing in the ear (tinnitus), fatigue, irritability, fainting and pain throughout the body. In order to feel improvement, some people have moved into remote areas however, it is difficult to avoid wireless signals no matter where one lives on the planet.

A Very Controversial Subject
Although studies relating to cellphones were inconclusive in the past, most of them were conducted by the cellular industry, and independent researchers have claimed foul play. However, people are increasingly speaking out because they are being affected. It is not unreasonable to think that the molecules of the human brain and body can be disturbed by the thousands of signals passing through them every second from AM, FM and HD Radio, satellites (TV, radio, GPS), cellular voice and data, cordless phones, radar, smart electric meters, Bluetooth (headphones, speakers, keyboards, mice) and especially the myriad applications of Wi-Fi.

When people around the world swear they feel better after moving from the city to a rural location or when shutting down their Wi-Fi, it is reasonable to think that electromagnetic hypersensitivity (EHS) is very real. We humans have genetic differences that can result in different reactions to the environment. Some may be very sensitive to radiation, while others are not. However, this is the first generation raised from infancy that is bombarded with wireless in such profusion, which has increased exponentially since the turn of the century. The higher frequencies of upcoming 5G cellular networks are also causing a lot of apprehension (see 5G radiation).

Duration and Constant Frequencies
Duration is one of two major reasons why radiation can be so harmful. People are bombarded 24/7 with manmade signals that emanate outside the home, and household members stream TV and premium channels via Wi-Fi for hours on end inside the home. The second reason is that manmade signals transmit as uniform frequencies in contrast to atmospheric radiation that is more random. The randomness is less harmful to human cells.

As a precaution when telephoning, many people turn the speaker on and hold the phone away from their head, or they use a wired headset. Even better are headsets with less wire (see air tube headset). Rather than stream video via Wi-Fi, households have switched from wireless to wired, running Ethernet cables from their router to their home theater equipment.

The constant beaconing in the Wi-Fi access point, which advertises the name of the Wi-Fi network all day long, can be easily turned off (see SSID broadcast). In addition, Wi-Fi routers and access points can be turned off at night with a timer while people sleep (see wireless router and PoE injector). In 2014, France took a major step by banning Wi-Fi entirely in nursery schools and turning Wi-Fi off in elementary schools when not specifically used for teaching. See SAR.

An Electromagnetic Field (EMF) Meter
Walking around the house with this meter can be very disturbing. When placed next to a Wi-Fi access point, the meter reaches the top 6.00 level and switches from yellow to red. Its audio output clicks faster as the radiation increases.

Wireless Wake-up Call
Working in Silicon Valley with a masters degree in engineering, Jeromy Johnson is an expert on EMF radiation. His 2016 TEDx Talk on the subject entitled a Wireless Wake-up Call is alarming but also informative, outlining ways people can prevent harmful exposure. For more information, visit

Very Educational
Radiation Nation contains a lot of worthwhile information about electromagnetic hypersensitivity, including tips on how to diminish exposure to EMF radiation. The author started DefenderShield, a company that makes products that minimize radiation (

Chapter 11: Hypersensitivity, Disorders Caused by Immune Responses

Antibody mediated: Antibodies specific for cell or tissue antigens can cause damage by activating complement and engaging phagocytes (type II hypersensitivity) antibodies can also destroy circulating cells and block essential molecules or their receptors.

Antibody-antigen complexes (immune complexes) deposit in blood vessels, causing inflammation and thrombosis, leading to tissue injury (type III hypersensitivity).

T cell mediated: Reactions of T lymphocytes, often against self antigens in tissues, can cause inflammation and tissue damage (type IV hypersensitivity/delayed hypersensitivity).

Exposure to an environmental antigen induces differentiation of IL-4 producing helper T cells, which in turn induce IgE antibody responses to the same antigen. The IgE binds to high-affinity IgE receptors (FceRI) on mast cells in tissues throughout the body. On subsequent exposure to the same antigen, the mast cell-bound IgE molecules bind the antigen and become cross-linked, generating signals from the associated Fcε receptors that lead to mast cell granule release, enzymatic generation of leukotrienes and prostaglandins, and synthesis of cytokines. Vasoactive amines such as histamine, released from the granules, and prostaglandins cause acute vascular changes leading to increased blood vessel permeability and edema, usually within minutes of exposure to the antigen.

The late-phase reaction is an inflammatory response in which blood leukocytes are recruited to the site of mast cell degranulation, caused by TNF and other cytokines secreted by the mast cells.

What are some examples of diseases caused by antibodies specific for cell surface or tissue matrix antigens?

Fig 11.8: Antibodies cause disease by A, inducing inflammation at the site of deposition B, opsonizing cells for phagocytosis and C, interfering with normal cellular functions, such as hormone receptor signaling. All three mechanisms are seen with antibodies that bind directly to their target antigens, but immune complexes cause disease mainly by inducing inflammation (A). TSH, Thyroid-stimulating hormone.

Thrombocytopenia or anemia caused by antibodies specific for platelet or red cell membrane proteins
Blistering diseases such as pemphigus vulgaris, caused by antibodies against cell adhesion proteins on skin keratinocytes.
Myasthenia gravis, loss of muscle function results from antibodies specific for the acetylcholine receptor.
In rheumatic fever, cardiac inflammation is caused by an antibody specific for a streptococcal bacterial antigen that cross-reacts with a myocardial antigen.

History and Physical

The clinical features associated with type IV hypersensitivity are variable and categorized into distinct clinical conditions, each with their own unique features.

Contact dermatitis occurs after the skin is exposed to an allergen (topical medication, poison ivy) and, over a period of time, develops into a very erythematous pruritic rash, often with swelling and edema progressing to vesicles and bullae. Some of these vesicles and bullae can rupture with subsequent crust formation. When the reaction is prolonged with lichenification and scaling, the condition can be termed as subacute or chronic contact dermatitis. Some of the agents implicated in the development of contact dermatitis include gloves, clothing, acrylics, preservatives, and an array of industrial chemicals. It is, therefore, prudent to ask the patients about their occupations, hobbies, and daily activities. 

Granulomatous-type hypersensitivity can be seen in tuberculosis and sarcoidosis. Sarcoidosis is considered as a granulomatosis entity with unknown cause, with a systemic involvement of any organ in the body. It results in the formation of granulomas by the immune system in affected organs. The most frequent organs to be affected in sarcoidosis are the lymphatic system, especially in the mediastinum, lungs, eyes, and skin. In 20% to 50% of the cases, ophthalmic involvement is found. Moreover, up to 30% of patients can present with non-specific symptoms, such as weakness, weight loss, or fever. When the lungs are affected, patients usually present with shortness of breath, breathing difficulty, dry cough, and chest pain. Occasionally, these symptoms progress to pulmonary fibrosis, with a progressive decline in pulmonary functions.[16][17]

Acute generalized exanthematous pustulosis (AGEP) is a rare drug reaction presenting as generalized pustular rash manifesting within 24 hours after exposure to an offending drug.

Drug fever:ꃎrtain drugs such as trimethoprim-sulfamethoxazole or tetracyclines can cause fever as the only manifestation, and certain conditions appear to increase this susceptibility when exposed to certain drugs. Patients with acute human immunodeficiency virus (HIV) infection are more prone to get drug fever when treated with antiretroviral therapy.

Stevens-Johnson syndrome/toxic epidermal necrolysis: These are life-threatening conditions that present with severe skin and mucosal necrosis with fluid losses and can present with hypovolemic shock. There is severe blistering of the skin with pain, sloughing of the epidermis that resembles a third-degree burn. Commonly implicated agents are nonsteroidal anti-inflammatory drugs (NSAIDs), anticonvulsants, and sulfa drugs. 

Drug-induced hypersensitivity syndrome (DiHS) is another severe drug-induced type IV hypersensitivity reaction presenting with rash, fever, and multiorgan involvement, particularly the heart, lungs, liver, and kidneys.

16.3 Modes of Disease Transmission

Understanding how infectious pathogens spread is critical to preventing infectious disease. Many pathogens require a living host to survive, while others may be able to persist in a dormant state outside of a living host. But having infected one host, all pathogens must also have a mechanism of transfer from one host to another or they will die when their host dies. Pathogens often have elaborate adaptations to exploit host biology, behavior, and ecology to live in and move between hosts. Hosts have evolved defenses against pathogens, but because their rates of evolution are typically slower than their pathogens (because their generation times are longer), hosts are usually at an evolutionary disadvantage. This section will explore where pathogens survive—both inside and outside hosts—and some of the many ways they move from one host to another.

Reservoirs and Carriers

For pathogens to persist over long periods of time they require reservoir s where they normally reside. Reservoirs can be living organisms or nonliving sites. Nonliving reservoirs can include soil and water in the environment. These may naturally harbor the organism because it may grow in that environment. These environments may also become contaminated with pathogens in human feces, pathogens shed by intermediate hosts, or pathogens contained in the remains of intermediate hosts.

Pathogens may have mechanisms of dormancy or resilience that allow them to survive (but typically not to reproduce) for varying periods of time in nonliving environments. For example, Clostridium tetani survives in the soil and in the presence of oxygen as a resistant endospore. Although many viruses are soon destroyed once in contact with air, water, or other non-physiological conditions, certain types are capable of persisting outside of a living cell for varying amounts of time. For example, a study that looked at the ability of influenza viruses to infect a cell culture after varying amounts of time on a banknote showed survival times from 48 hours to 17 days, depending on how they were deposited on the banknote. 8 On the other hand, cold-causing rhinoviruses are somewhat fragile, typically surviving less than a day outside of physiological fluids.

A human acting as a reservoir of a pathogen may or may not be capable of transmitting the pathogen, depending on the stage of infection and the pathogen. To help prevent the spread of disease among school children, the CDC has developed guidelines based on the risk of transmission during the course of the disease. For example, children with chickenpox are considered contagious for five days from the start of the rash, whereas children with most gastrointestinal illnesses should be kept home for 24 hours after the symptoms disappear.

An individual capable of transmitting a pathogen without displaying symptoms is referred to as a carrier. A passive carrier is contaminated with the pathogen and can mechanically transmit it to another host however, a passive carrier is not infected. For example, a health-care professional who fails to wash his hands after seeing a patient harboring an infectious agent could become a passive carrier, transmitting the pathogen to another patient who becomes infected.

By contrast, an active carrier is an infected individual who can transmit the disease to others. An active carrier may or may not exhibit signs or symptoms of infection. For example, active carriers may transmit the disease during the incubation period (before they show signs and symptoms) or the period of convalescence (after symptoms have subsided). Active carriers who do not present signs or symptoms of disease despite infection are called asymptomatic carrier s. Pathogens such as hepatitis B virus , herpes simplex virus , and HIV are frequently transmitted by asymptomatic carriers. Mary Mallon , better known as Typhoid Mary , is a famous historical example of an asymptomatic carrier. An Irish immigrant, Mallon worked as a cook for households in and around New York City between 1900 and 1915. In each household, the residents developed typhoid fever (caused by Salmonella typhi ) a few weeks after Mallon started working. Later investigations determined that Mallon was responsible for at least 122 cases of typhoid fever, five of which were fatal. 9 See Eye on Ethics: Typhoid Mary for more about the Mallon case.

A pathogen may have more than one living reservoir. In zoonotic diseases, animals act as reservoirs of human disease and transmit the infectious agent to humans through direct or indirect contact. In some cases, the disease also affects the animal, but in other cases the animal is asymptomatic.

In parasitic infections, the parasite’s preferred host is called the definitive host . In parasites with complex life cycles, the definitive host is the host in which the parasite reaches sexual maturity. Some parasites may also infect one or more intermediate host s in which the parasite goes through several immature life cycle stages or reproduces asexually.

Link to Learning

George Soper, the sanitary engineer who traced the typhoid outbreak to Mary Mallon, gives an account of his investigation, an example of descriptive epidemiology, in “The Curious Career of Typhoid Mary.”

Clinical Findings:

Chronic cough is the most common sign. It may be mild or severe, productive or nonproductive, and progressive or nonprogressive. Weight loss, tachypnea, dyspnea, wheezing, exercise intolerance, and occasionally hemoptysis may be seen. Severely affected animals may exhibit moderate to severe dyspnea and cyanosis at rest. Auscultation varies from unremarkable to increased breath sounds, crackles, or wheezes. Fever is usually absent. The degree of dyspnea and coughing is related to the severity of inflammation within the airways and alveoli.

Immunity Types: 3 Main Types of Immunity | Immunology

The following points highlight the three main types of immunity present in humans. The types are: 1. Innate (Natural or Nonspecific) Immunity 2. Acquired (Specific or Adaptive) Immunity 3. Active and Passive Immunity.

Type # 1. Innate (Natural or Nonspecific) Immunity:

Innate immunity (also called nonspecific or natural immunity) refers to the inborn-ability of the body to resist, and is genetically transmitted from one generation to the next. This immunity offers resistance to any microorganism or foreign material encountered by the host.

It includes general mechanisms inherited as part of the innate structure and function of each vertebrate, and acts as first line of defence. Innate immunity lacks immunological memory, i.e., it occurs to the same extent each time a microorganism or foreign material is encountered.

Types of Innate Immunity:

Innate immunity can be divided into species, racial, and individual immunity.

Species immunity (species resistance) is that in which a disease affecting one species does not affect the other species. For convenience, humans do not contract cattle plague, chicken cholera, hog cholera, infectious horse anaemia, etc., while animals are not affected by many human diseases such as enteric fever, scarlet fever, syphilis, gonorrhoea, measles, etc.

Diseases of skin, to which humans are quite susceptible, are often resisted by animals because they have more hair and thicker hides. Species resistance is considered to be the result of a long evolution of interactions between the highly evolved “macro” organisms and the pathogenic microorganisms.

(ii) Racial Immunity:

Racial immunity (racial resistance) is that in which various races (breeds) show marked differences in their resistance to certain infectious diseases. A well known example is that Brahman cattle are resistant to the protozoan parasite responsible for tick fever in other breeds of cattle. Similarly, Black Africans affected by sickle cell anaemia, a genetic disease, are resistant to malaria while malaria affects other human races.

(iii) Individual Immunity:

Having the same racial background and opportunity for exposure, some individuals of the race experience fewer or less severe infections than other individuals of the same race. For convenience, children are more susceptible to diseases such as measles and chicken pox, while aged individuals are susceptible to other diseases like pneumonia.

Type # 2. Acquired (Specific or Adaptive) Immunity:

Acquired immunity (also called specific or adaptive immunity) refers to an immunity that is developed by the host in its body after exposure to a suitable antigen or after transfer of antibodies or lymphocytes from an immune donor.

Characteristics of Acquired Immunity:

Acquired immunity is highly adaptive and is capable of specifically recognizing and selectively eliminating foreign microorganisms and macromolecules, i.e., antigens.

It exhibits the following four characteristic features that distinguish it from nonspecific (innate) immunity:

Acquired immunity is extremely antigenic specific as it acts against a particular microbial pathogen or foreign macromolecule and immunity to this antigen usually does not confer resistance to others. For convenience, the ability of the antibodies to differentiate between antigen molecules differs even by a single amino acid.

The acquired immune system generates tremendous diversity in its recognition molecules. As a result, it is able to specifically recognise billions of different structures on foreign antigens.

Once the acquired immune system has recognised and responded to an antigen, it is able to respond this antigen more quickly and strongly following a subsequent exposure. This is due to the constitution of immunologic memory that makes the basis for long-term immunity in the body of the host.

(iv) Discrimination between “Self’ and “Nonself”:

The immune system almost always recognizes self and nonself antigens and responds only to nonself antigens. This ability to recognize self antigens from nonself ones is critical for normal functioning of the immune system. Sometimes this feature fails and, as a result, there develops autoimmune disease in the host.

Major Functions of Acquired immunity:

The acquired (specific or adaptive) immune system of the body is required to perform the following three major functions:

(i) It has to recognize any thing that is foreign to the body. The foreign material is called “nonself”. The recognition system of acquired immunity is so highly specific that it is able to differentiate one pathogen from another, cancer cells, and even body’s own “self” proteins from foreign “nonself” proteins.

(ii) After recognizing the foreign invader, the acquired immune system responds to this invader by recruiting its defensive molecules and cells to attack the invader. This response, called effector response, either eliminates the invader or makes it harmless to the host and thus protects the body from disease.

(iii) The acquired immune system remembers the foreign invader even after its first encounter. If the same invader attacks the previously attacked body at a later time, the system remembers the invader and mounts a more intense and rapid memory or anamnestic response, which ones again eliminates the invader and protects the host from disease.

Components of Acquired Immunity:

Acquired immunity involves the following two major groups of cells:

(2) antigen-presenting cells (APCs).

Lymphocytes are one of the many types of white blood cells (leucocytes) generated in bone marrow by the process of hematopoiesis. They migrate from bone marrow, circulate in the blood and lymphatic system, and reside in various lymphoid organs.

Lymphocytes possess antigen-binding cell-surface receptors and are responsible for the specificity, diversity, memory, and self/nonself recognition by the immune system.

In contrast, antigen-presenting cells (APCs) have class II MHC (major histocompatibility complex) molecules on their plasma membrane. These MHC molecules bind to antigen-derived peptides and present them to a group of lymphocytes, which are then activated to mount the immune response.

Collaboration between Innate and Acquired Immunities:

Although the acquired immunity develops after exposure to a suitable antigen or after transfer of antibodies or lymphocytes from an immune donor, it is not independent of innate immunity which is an inborn ability in the body.

Both the immunities function as a highly interactive and cooperative system rendering a combined response more effective than either immunity could produce by itself. It so happens because certain immune components play significant role in both types of immunities.

Following are the examples that show the interactive and cooperative roles of the two immunities:

(i) Phagocytic cells crucial to innate immunity are intimately involved in activating acquired immunity. Interactions between receptors on phagocytic cells and microbial components generate soluble factors that stimulate and direct acquired immunity facilitating the participation of the system in the elimination of the foreign invader. Acquired immune system, in turn, produces signals and components that stimulate and inhance the effectiveness of innate immunity.

(ii) Stimulated phagocytic cells involved in innate immunity also secrete cytokines that direct acquired immunity against particular intracellular microbial pathogens. In turn, some T lymphocytes of acquired immunity synthesize and secrete cytokines that increase the ability of phagocytic cells to destroy the microbial pathogens they have phagocytized during innate immune responses.

Differences between Innate and Acquired Immunities:

In contrast to their interactive and cooperative nature, the innate and acquired immunities show certain fundamental differences, which are the following:

(i) Innate immunity shows rapid response in comparison to acquired immunity the response of which is slower.

(ii) Innate immunity utilizes a pre-existing but limited repertoire of responding components, whereas the acquired immunity possesses ability to recognize a much wider repertoire of foreign substances.

(iii) Innate immunity remains constant during a response, whereas the acquired immunity possesses ability to improve during the response. It may be emphasized that due to its immunological memory, the acquired immunity operates much faster to the same pathogen during secondary exposure than the primary exposure.

These fundamental differences between innate and acquired immunity can be consolidated in the form of Table 41.2.

Types of Acquired Immunity:

Acquired immunity can be obtained by the host actively or passively and, on this basis, can be categorized as of two types:

In active immunity, there is active involvement of host’s own immune system leading to the synthesis of antibodies and/or the production of immuno-competent cells (ICCs).

In passive immunity, on the contrary, the antibodies and /or the immuno-competent cells (ICCs) are transferred from one host to another. Active and passive immunities can be obtained naturally or artificially (Fig. 41.1).

Branches or Arms of Acquired Immunity:

Acquired immunity consists of two branches or arms recognized as:

Humoral immunity is based on the action of soluble proteins called ‘antibodies’ whereas cellular immunity is based on the action of specific kinds of ‘T lymphocytes’.

Type # 3. Active and Passive Immunity:

1. Active Immunity:

Active immunity, as stated earlier, refers to an immunity in which there is active involvement of host’s own immune system leading to the synthesis of antibodies and/or the production of immunocompetent cells (ICCs).

There are two types of active immunity:

(i) Naturally acquired active immunity and

(ii) Artificially acquired passive immunity.

(i) Naturally Acquired Active Immunity:

This immunity develops after antigens (e.g., microbial pathogens) enter the body by natural processes such as infection and, in response, the body’s immune system forms antibodies.

In some cases, the immunity may be life-long as with smallpox, measles, chickenpox, yellow fever etc. In other cases, however, the immunity may be lost after only a few years (e.g., diphtheria, tetanus) or even for lesser period (e.g., influenza, pneumonia).

(ii) Artificially Acquired Active Immunity:

When a carefully chosen antigen (e.g., vaccine, chemically altered toxins called toxoids) is intentionally introduced into a body to be immunized, the latter develops immunity that is called artificially acquired active immunity. This immunity is artificial because the antigens are intentionally or purposely introduced, and it is active because the recipient’s immune system synthesizes antibodies in response.

Vaccines provide usually long-term immunity. Vaccines are now available against many infectious diseases such as cholera, tuberculosis, plague, pneumonia, rocky mountain spotted fever, smallpox, polio, tetanus, influenza, measles, rabies, yellow fever etc. Toxoids are currently available for protection against diphtheria and tetanus, the two diseases whose major effects are due to toxins.

The characteristics of naturally acquired and artificially acquired active immunities are summarized in Table 41.3.

2. Passive Immunity:

Passive immunity, as stated earlier, refers to an immunity in which the antibodies and/or immuno-competent cells (ICCs) are transferred from one host to another.

There are two types of passive immunity:

(i) Naturally acquired passive immunity and

(ii) Artificially acquired passive immunity.

(i) Naturally Acquired Passive Immunity:

When antibodies produced in the body of an individual (called “donor”) are naturally transferred into the body of other individual (called “recipient”), the latter develops immunity, called naturally acquired passive immunity, in its immune system.

This immunity is natural because the transfer of antibodies from donor to recipient occurs under natural conditions, and it is passive because the recipient does not synthesize antibodies but picks them up from the donor.

The best example of this type of immunity is the natural transfer of antibodies from the mother to the foetus across- the placenta. Certain antibodies are also transferred from mother to infant through colostrum and milk during nursing.

These antibodies, called maternal antibodies, remain with the child for about three to six months or, sometimes, twelve to fifteen months, and after the specified time the immune state disappears. The maternal antibodies generally provide resistance against whooping cough, diphtheria, german measles, diseases of respiratory and gastrointestinal tract, etc.

(ii) Artificially Acquired Passive Immunity:

Artificially acquired passive immunity is that which develops as a result of the intentional introduction of antibody-rich serum (blood plasma devoid of clotting factors) taken from diseased individual to another susceptible individual.

It was an important therapeutic device for disease treatment before the vaccines were developed and is still used for viral diseases such as hepatitis B, chicken pox, arthropod-borne encephalitis, and for bacterial diseases such as botulism, diphtheria, tetanus, staphylococcal-poisoning where toxins are involved in disease causation.

Since these diseases are very dangerous and fatal, already-made antibodies present in serum are introduced into the blood of the susceptible individual for quick response and no risk is taken for introduction of antigens. Artificially acquired passive immunity is immediate but short-lived (only for two to three weeks).

The characteristics of naturally acquired and artificially acquired passive immunities are summarized in Table 41.4.

Watch the video: ΑΘΛΗΤΙΑΤΡΙΚΗ 12 Απριλίου 2021 (July 2022).


  1. Giannes

    I recommend that you visit a site that has many articles on this subject.

  2. Dourn

    In my opinion, he is wrong.

  3. Placido

    It is remarkable, rather the helpful information

  4. Akidal

    It is true! I think this is a good idea. Fully agree with her.

Write a message