What is immune System? Its Facts, Mechanisms & Function

Immune system

It is the organ system which gives an ability for the organism to resist particular infections or toxins by the specific action of antibodies or sensitized white blood cells.

The immune system is, the way of body fighting to protect against any infections.

When your body is infected by any diseases of bacteria, viruses or parasites, it indicates compromised immune status.

The immune system which is comprised of special cells, organs and tissues. The immune system is works by antigen-antibodies reactions.

Antigen:   it is a substance, usually protein in nature. Which introduced the tissue stimulates for antibody production.

Hapten:   it is a non-protein substance, which has no antigenic properties.

Antibody: it is a protein substance which binds to an antigen, there are 5 classes: IgG, IgA, IgM, IgE, and IgD.

The immune system may combine with antibodies to form antigen-antibodies complexes.

Types of Immunity

The immune system is broadly divided into two types.

  1. Natural or innate immunity
  2. Specific or adaptive immunity

It is a non-specific and is characterized by the without antigenic specificity.it has two major components.

  1. Humoral: comprised by complements
  2. Cellular: it consists of macrophages, neutrophills, and naturalkiller (nk) cells

It is a specific and is mainly characterized by the antigenic specificity.it has two major components.

a. humoral: consists of macrophages by specified T cells

b.cellular: mediated T cells.

Structure of immune system

The structure of immune system is two types.

  1. Organ immune system
  2. Cellular immune system

Organ immune system

The organ of immune system is distributed by different places. The organ of immune system is described in this below.

Primary lymphoid organs: thymus, Bone marrow

Secondary lymphoid organs: lymph nodes, Spleen

MALT (mucosa-associated lymphoid tissue)

Cells of immune system

The cell of immune system is various components.

Monocytes and macrophages






What is immunity

Mechanism of immunity

Antigen recognition: They possess cell surface receptors to several extracellular molecules receptor for cytokines, selectin, integrins and fc(constant fragment of antibody.these receptor recognize the organism and initiate intracellular mechanism in macrophages. The antigen become recognizable can also get coated by antibodies or complement. this process is being termed as opsonisation.

Phagocytosis: the Phagocytosis is defined as the process of engulfment of solid particulate material by the cells (cell-eating).the cells of  performing this function are called phagocytes. There are two main types of phagocytic cells.

  1. polymorphonuclearneutrophils (pmns): which appears early in acute inflammatory response, sometimes called as microphages.
  2. Circulating monocytes and fixed tissue mononuclear Phagocytes commonly called as macrophages.

Secretory function: macrophages secrete important biomolecule substance as follows.

  1. Cytokines (IL-1,IL-2,IL-6,IL-8,IL-10,IL-12,Tumour necrosis factor-α)and prostaglandins(PGE,Thromboxane-A,leukotrienes)which are chemical mediators of activates other leukocytes.
  2. Secretory protein involved in wound healing e, g. collagenase, elastase, fibroblast growth factor, angiogenesis factor.
  • Acute phase reactants e.g. fibronectin, microglobulin.

Antigen presentation: The macrophages are unable to lyse an antigen or an organism,the next best course adopted by them is to act as antigen-presenting cells for presenting to immunocompetent T cells(subtype CD4+ OR CD8+ cells),or to B cells.

Basophils and mast cells:Basophils are a type of circulating granulocytes(0-1%)while mast cells are their counterpart seen in tissues, especially in connective tissues around blood vessels and submucosallocationBasophiles and mast cells have IgE surface receptor thus on coming in contact with antigen binding to IgE(e.g. allergic reaction and parasites),these cells get activated and release granules i.e.degranulate.these granules contain substances suchas:Histamine,platelate activating factor, heparin and certain chemical mediators.

Mast cells and basophiles are involved in mediating inflammation in allergic reactions and have a role in wound healing.

Neutrophils:polymorphonuclearneutrophils (PMNs) are normally the most numerous of the circulating leucocytes (40-75%).the cytoplasm of the OMNs contains lysosomal granules of three types: primary, secondary, tertiary. The PMNs function as similar to macrophages and are therefore appropriately reffered to as microphages owing to their role as frist line of defense against an invading forgein organism in the body.the cells have limitation size and type of organisms to be engulfed.

Eosinophils: The Eosinophils are also circulating granulocytes(1-6%).these cells play a role in allergic reaction and in intestinal helminthiasis.the granules of Eosinophils contain lysosomal enzymes,peroxidases,and chemical mediators of inflammation(e.g.prostaglandins,leukotrenes).

Diseases of immunity:

The disease of immune system is broadly classified into the following four categories.

  1. Immunodeficiency disorders
  2. Hypersensitivity reaction
  • Autoimmune diseases

Immunodeficiency disorders:

Failure or deficiency of immune system, which normally plays a protective role against infections. The deficiency diseases are classified into 2 types.

  1. Primary Immunodeficiencies: It is usually the result of genetic or developmental abnormality of the immune system.

Secondary Immunodeficiencies: It arise from acquired suppression of the immune system

The increasing number of primary and secondary Immunodeficiency syndrome are being added to the list, the latest addition being the acquired immunodeficiency syndrome.

A.primary Immunodeficiency diseases

  1. Severe combined Immunodeficiency diseases:

I.Recticular dysgenesis                  Failure to develop primitive marrow reticular cells.

II.Thymiclymphoplasia                No lymphoid stem cells.

III.Agamma-globulinaemia            No lymphoid stem cells.

IV.Wiscott-Aldrich syndrome     associated feature are thrombocytopenia and eczema defective Tcell maturation.

  1. T-cell defect: Epithelial component of thymus fails to develop
  2. B cell defects (antibody deficiency diseases):

I.Brutons x-linked agammaglobulinaemia                   Defective differentiation from pre-B to B cells

II.Autosomal recessive agammaglobulinaemia                 Defective differentiation from pre-B to B cells

III.IgA deficiency                                                                   Defective maturation of IgA synsthesising B cells

IV.Selective deficiency of other Ig types                           Defective differentiation from Bcells to specific Ig-synthesising plasma cells

V.Immune deficiency with thymoma                                 Defective pre-B cell maturation

  1. Common variable immunodeficiencies
  2. With predominant B cell defect Defective differentiation of pre-B to mature B cells

II.With predominant T cell

A.Deficient T helper cells                                              Defective differentiation of thymocytes to T helper cells

B.Presence of activated T suppressor cells                     T cell disorder of unknown origin

III.With autoantibodies to B and T cells                          Unknown differentiation defect

B.Secondary immunodeficiency diseases

1.infections                                                                        AIDS (HIV viruses);other viral,bacterial and protozoal infections

2.Cancer                                                                              Chemotherapy by antimetabolites irradiation

3.Lymphoid neoplasms                                                    Defective T and B cell functions

4.Malneutrition                                                                 Protein deficiency

5.Sarcoidosis                                                                      Impaired T cell function

  1. Autoimmune diseases Administration of high dose of steroids toxic to lymphocytes
  2. Transplant cases Immunosuppressive therapy

Pathogenesis: types

The pathogenesis of HIV infection is largely related to the deplectionof CD+T cells)resulting profound immunosuppression. The sequence of events shown schematically is outlined below:

  1. Selective tropism for CD4 molecule receptor:gp 120 envelope glycoprotein of HIV has selective tropism for cells containg CD4 molecule receptor on their surface. These cells mostly importantly are CD4+T cells(T helper cells) other such cells include monocyte-macrophages, microglialcells, epithelial cells of the cervix, Langerhans cells of the skin and follicular dendritic cells. Initially, HIV on entering the body via route described above has tropism for macrophages (M-tropic)which later it becomes either dual tropic or T-tropic only and thus affects mainly CD4+T cells which are the main target of attack by HIV.
  2. Internalisation:gp 120of the virion combines with CD4 receptor, but for fusion of virion with the host cell membrane, a chemokine coreceptor (CCR) is necessary. Once HIV has combined with CD4 receptor and CCR, gp41 glycoprotein of envelope is internalized in the CD4+ T cell membrane.
  3. Uncoating and viral DNA formation: Once the virion has entered the T cell cytoplasm, reverse transcriptase of the viral RNA forms a single-stranded DNA.Using the single-stranded DNA as a templete, DNA polymerase copies it to make it double-stranded DNA, while destroying the original RNA strands .Viral DNA so formed has frequent mutations making the HIV quite resistant to anti-viral therapy.
  4. Viral integration: The viral DNA so formed may initially remain unintegrated in the affected cell but later viral integrase protein inserts in the host cell DNA.At this stage viral particle is termed as HIV provirus.
  5. Viral replication :HIV provirus having become part of host cell DNA ,host cell DNA transcripts for viral RNA with presence of tat gene .multiplication of viral particles is further facilitated by release of cytokines from T helper cells (CD4+T cells)TH1 cells elaborating IL-2 and IFN-γ, and TH 2 cells elaborating IL-4,IL-5,IL-6,IL-10.RNA viral particles thus fill the cytoplasm of host T cell from where they acquire protein coating .
  6. Latent period and immune attack: In an inactive infected T cell, they infection may remain in latent phase for a long time ,accounting for the long incubation period, Immune system does act against the virus by participation of CD4+ and CD8+T cells, macrophages and by formation of antibodies to mount attack against the virus. However, this period is short and the virus soon overpowers the host immune system.
  7. CD4+T cell destruction: Viral particles replicated in the CD4+T cells starts forming buds from the cell wall of the host cell. As these particles detach from the infected host cell, they precusors of CD4+ cells by the virus and by formation of syncytial gaint cells due to attachment of more and more of gp 120 molecules to the surface of CD4+ T cells.
  8. Viral dissemination: Release of viral particles from infected host cell spreads the infection to more CD4+host cells and produces viraemia.
  9. Impact of HIV infection on their immune cells: HIV infects other cells of the host immune system and also affects non-infected lymphoid cells.
  10. HIV infection of nervous system: out of non-lymphoid organ involment,HIV infection of nervous system is the most serious and 75-90% of AIDS patients may demonstrate some form of neurological involvement at autopsy. It infects microglial cells ,astrocytes and oligodendrocytes as under:
  11. Infection carried to the microglia of the nervous system by HIV infected CD4+ monocyte-macrophage subpopulation or endothelial cells.
  12. Direct infection of astrocytes and oligodendrocytes.

III.Neurons are not invaded by HIV but are affected due to attachment of gp 120 and by release of cytokines by HIV–infected macrophages.

Major abnormalities immune system in AIDS

  2. I. Lymphopenia

II.CD4+T cell deplection

III.CD8+T cell lymphocytosis

IV.Reversed of CD4:CD8 cell ratio

  1. Decreased production of cytokines by CD4+T cells

VI. Decresed antibody-depended cellar cytotoxicity (ADCC) BY CD8+T cells


I.NO direct viral damage

II.Decresed Ig production

III.Polyclonal activation


V.Circulating immune complexes

  2. No direct viral damage

II.Depressed number

III.Decresed cytotoxicity

  2. No destruction

II.Decresed chemotaxis

III.Decresed cytotoxicity

Hypersensitivity reactions:

Hypersensitivity reaction is defined as a exaggerated or inappropriate state of normal immune response with onset of adverse effects on the body. The lesion of hypersensitivity are aform of antigen-antibody reaction. These lesions are termed as  hypersensitivity reaction or immunologic tissue injury. Thehypersensivity reaction is broadly divided into four types: Type I, II, III, IV.its depends on the rapidity, duration and type of the immune response. These four types of hypersensitivity reactions are grouped into two types.

  1. Immediate
  2. Delayed
  3. Immediate:

            The administration of antigen, the reaction occurs immediately (within seconds to minutes.) the Immune response in this type is immediate largely by humoral antibodies. The immediate type of hypersensitivity reactions included type I, II, III.

  1. Delayed:

This reaction is slower in onset and develops within 24-48 hours and the effect is prolonged. It is immediate by cellular response (T cell mediated) and it included type IV reaction.

The mechanisms and examples of immunologic tissue injury by the 4 types of hypersensitivity reactions are summarized.

Type I: Anaphylactic (Atopic) Reaction

Type I hypersensitivity is defined as a state of rapidly developing or anaphylactic type of immune response to antigen to which the individual is previously sensitized (anaphylaxis is the opposite of prophylaxis).The reaction appers within 15-30 minutes of exposure to antigen.


Type I reaction includes participation by B lymphocytes and plasma cells, mast cells and basophils, neutrophils and eosinphils.The mechanism briefly discussed in below.

  1. Duration the first contact of the host with the antigen, sensitization takes place. In response initial contact with antigen, circulating B lymphocytes get activated and differentiate to form IgE secreting plasma cells. IgE antibodies so formed bind to the fc receptors present in plenty on the surface of mast cells and basophils, which are the main effector cell soft type I reaction.

II.During the second contact with the same antigen, IgE antibodies on the surface of mast cells-basophils are so firmly bound to fc receptors that it sets in cells damage membrane lysis influx of sodium and water and degranulation of mast cells basophils.

III.The released granules contain important chemicals and enzymes with proinflammatory properties histamine,serotonine,vasoactive intestinal peptide (VIP) chemotactic factors of anaphylaxis for neutrophils and basophils,leukotrines B4 and D4,prostaglandins and platelet activating factor. The effects of these agents are:

Increased vascular permeability

Smooth muscle contraction

Early vasoconstriction followed by vasodilation



Increased nasal and lacrimal secretions

Increased migration of eosinophils and neutrophils at the site of local injury as well as their rise in blood(eosinophilia and neutrophilia).

Type II: Cytotoxic (cytolytic) reaction

Type II or cytotoxic reaction is defined as reactions by humoral antibodies that attack cell surface antigens on the specific cells and tissue cause lysis of target cells. Type II reaction is appears generally within 15-30 minutes. It may appear after longer duration.


In general type II reactions have participation by complement system, tissuemacrophages, platelets, natural killer cells, neutrophils and eosinophils while main antibodies are IgG, and IgM.Type II hypersensitivity is tissue specific and reaction occurs after antibodies bind to tissue specific antigens, mostoften on blood cells. The mechanism involved is as under

  1. The antigen on thesurface of target cell (foreign cell)attracts and binds fab portion of the antibody(IgGand IgM) forming antigen-antibody complex.

II.The unattached fc fragment of antibodies (IgG and IgM) forms a link between the antigen and complement.

III.The antigen-antibody binding with fc forming a link causes activation of classical pathway of serum complement which generates activated complement component, C3b, by splitting C4 and C2 by C1.

IV.Activated C3b bound to the target cell acts as an opsonin and attracts phagocytes to the site of cell injury and initiates phagocytosis.

Antigen-antibody complex also activates complement system and expose membrane attack complex(MAC)that attacks and destroys the target cell.

Type III:Immune complex mediated(arthus) reaction

Type III reactions result from deposition of antigen-antibody complexes on tissues which is followed by activation of the complement system and inflammatory reaction, resulting cell injury. The onset of type III reaction takes place about 6 hours after exposure to the antigen.


It may be mentioned here that both type II and type III reactions have antigen-antibody complex formation but the two can be distinguished antigen in type II is tissue specific while in type III is not so; moreover the mechanism of cell injury in type II is direct but in type III it is by deposition of antigen-antibody complex on tissues and subsequentsequace of cell injury takes place.

TypeIII reaction has participation by IgG and IgM antibodies, neutrophils, mast cells and complement. The sequence of underlying mechanism is as under

  1. Immune complexes are formed by interaction of soluble antibody and soluble or insoluble antigen.

II.Immune complexes which fails to get removed from body fluid get deposited into tissues. Generally, small and intermediated sized antibodies and antigens precipitate out of the body fluid get and get deposited in tissues.

III.Fc component of antibody links with complement and activates classical pathway of complement resulting in formation of C3a, C5a and membrane attack complex.

IV.C3a stimulate release of histamine from mast cells and its resultant effects of increased vascular permeability and oedema.

V.C5a releases proinflammatory mediators and chemotactic agents for neutrophils.

  1. Accumulated neutrophils and macrophages in the tissues release cytokines and result in tissue destruction.

Type IV: Delayed hypersensitivity (cell-mediated) reaction

Type IV or delayed hypersensitivity reaction is tissue injury by cell mediated immune response without formation of antibodies (contrary to type I, II, III)but it is instead a slow and prolonged response of specifically-sensitized T lymphocytes. The reaction occurs about 24 hours after exposure to antigen and the effect is prolonged which may last up to 14 days.


Type IV reaction involves role of mast cells and basophils, macrophages and CD8+T cells. The mechanism of type IV reaction is briefly discussed in below.

  1. The antigen is recognized by CD8+T cells (cytotoxic T cells) and is processed by antigen presenting cells.

II.Antigen-presenting cells migrate to lymph node where antigen is presented to T cells(CD+T cells)

III.Helper T cells release cytokines that stimulate T cell proliferation and activate macrophages.

IV.Activated T cells and macrophages release proinflamatory mediators and cause cell destruction.

Autoimmune diseases:

Autoimmunity is a state in which the body’s immune system fails to distinguish between self and non-self and reacts by formation of autoantibodies against one’s own tissue antigen. In other words there is a loss of tolerance to one’s own tissues autoimmunity is the opposite of immune tolerance. The Immune tolerance is defined as the ability of an individual to recognize self-tissue and antigens. Normally the immune system of the body is able to distinguish self from non-self-antigens by the following mechanisms:

  1. Clonal elimination: According to this theory during embryonic development T cell maturing in the thymus acquired the ability to distinguish self from non-self. These T cells are then eliminated by perforin apoptosis pathway for the tolerance individual.
  2. Concept of clonal energy: According to this mechanism T lymphocytes which acquired to ability to distinguish self from non-self are not eliminated but instead become non-responsive and inactive.
  3. Suppressor T cells: According to this mechanism, the tolerance is achieved by a population of specific suppressor T cells which do not allows the antigen-responsive cells to proliferate and differentiate.


The mechanism or theories of autoimmunity may be immunological, genetic, andmicrobial, all of which may be interacting.

  1. Immunological factors: Failure of immunological mechanisms of tolerance initiates autoimmunity .These mechanisms are as follows:
  2. Polyclonal activation of B cells:B cells may be directly activated by stimuli such as infection with microorganisms and their products leading to by passing of T cell tolerance.

II.Generation of self-reacting:B cell clones may also lead to by passing T cell tolerance.

III.Decresed T suppressor and increased T helper cell activity:Loss of T suppressor cell and increase in T helper cell activities  may lead to high levels of auto-antibody production by B cells contributing to autoimmunity.

IV.Fluctuation of anti-idiotype network control: may failure of mechanisms of immune tolerance.

  1. Sequestered antigen released from tissues:There is a formation of anti-sperm antibodies against spermatozoa similar is the formation of autoantibodies against lens crystalline.
  2. Genetic factors: There is a evidence in support of genetic factors in the pathogenesis of autoimmunity as under:
  3. Thereis increased expression of classII HLA antigens on tissues involved in autoimmunity.

II.There is increased familial incidence of some of the autoimmune disorders.

  1. Microbial factors:Infection with microorganisms, particularly viruses(e.g.EBV infection), and less often bacteria (e.g. streptococci, klebsiella) and mycoplasma, has been implicated in the pathogenesis of autoimmune diseases.

Drugs used in immune system:

  1. Calcineurin inhibitors(specific T-cell inhibitors)



  1. Antiproliferative drugs(cytotoxic drugs)






  1. Glucocorticoids


  1. Antibodies


Antithymocyte globulin

Rho (D) immunoglobulin


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