A state of balance in the immune responses (humoral or cell-mediated) is essential for protection against endogenous and exogenous antigens. Hypersensitivity is defined as a state of exaggerated immune response to an antigen. The lesions of hypersensitivity (immunologic tissue injury) are produced due to interaction between antigen and product of the immune response.

Depending upon the rapidity and duration the immune response, four distinct forms of hypersensitivity reactions are recognized:

Type I reaction: Immediate typein which on administration of antigen, the reaction occurs immediately (within seconds to minutes). Immune response in this type is mediated largely by humoral antibodies. Immediate type of hypersensitivity is further of three types — type I, II and III.

Immediate hypersensitivity reaction morphologically manifests by the picture of acute immune inflammation which develops rapidly, alteration and exudation stages prevail, proliferation increases slowly. The vessels and connective tissues are involved first. Alteration manifests by mucoid, fibrinoid swelling and fibrinoid necrosis. The exudate is either fibrinous or fibrino-hemorrhagic. Acute immune inflammations are observed in tuberculosis, syphilis. It is responsible for vascular reaction in lupus

erythematosus, glomerulonephritis, nodular periarteritis.

Type II reaction: antibody-mediated cytotoxicity.In this type, antibody reacts with a normal or altered cell-surface component, leading to subsequent destruction or inactivation of the target cell.

Type III reaction: immune complex disease.In this type of reaction, circulating antigen—antibody (immune) complexes (which normally are removed by the reticuloendothelial system) are deposited in tissues, leading to complement activation and further tissue injury. Immune complexes may also develop in situ (i.e., antibodies are directed against antigens that are endogenous to the tissues or have been planted there), thus triggering localized tissue damage.

Type IV reaction: cell-mediated hypersensitivity.Cell-mediated hypersensitivity reactions do not require the presence of antibody and, characteristically, are delayed anywhere from about 24 hours to 2 weeks. Three interrelated mechanisms are recognized, all of which involve activated T-cells.

Two types of cells take part in this reaction. They are sensibilized lymphocytes and macrophages. Morphologically it manifests by chronic immune inflammation characterized by lymphocyte-macro-phage infiltration. When we see lymphocyte-macro-phage infiltration accompanied by vascular plasmor-rhagic and degenerative processes we can conclude about immune inflammation. The condition occurs in

autoimmune diseases, tuberculosis, brucellosis, dermatitis.

Granulomatosis is morphological manifestation of slow hypersensitivity reaction.

Reaction of transplant rejectionresembles slow hypersensitivity reaction. Transplant antigens induce the production of antibodies and sensibilized lymphocytes which infiltrate the transplant.

Microscopically, lymphohistiocyte infiltration is observed in the transplant. Cellular infiltration causes the disturbance of blood circulation and edema, as a result degenerations and necrosis of transplant develop. The neutrophils and macrophages appear in the transplant. Enzyme destruction of the transplant begins which is followed by its rejection.


Immunologic tolerance and autoimmunity.An

immune response generated against self antigens is an aberrancy that implies a loss of immunologic ability to distinguish between self and nonself. The normal status of immunologic nonresponsiveness to self is termed tolerance.Tolerance probably represents an active process involving continuous generation of cellular and humoral inhibitory regulators. Loss of tolerance to self antigen is referred to as autoimmunity.The mechanisms by which tolerance is generated and lost are poorly understood. Theories of autoimmunity include:

1. Recognition of previously hidden or sequestered antigen.

2. Diminution of suppressor T-cell function.

3. Increase in helper T-cell activity.

4. T-cell-independent polyclonal B-cell activation by complex antigens.

5. Modification of self antigens by drugs or microorganisms.

6. Cross-reactivity between autologous antigens and microbial antigens.

Autoimmune diseases are those occurring as a result of the reaction of autoantibodies and sensibilized lymphocytes against normal antigens of the own tissue. The causes of autoimmune diseases are not clearly known. Chronic viral infections, radiation and genetic factors may be responsible for them.

Before studying the pathogenesis of autoimmune diseases it is necessary to know the major histocompatibility complex (MHC), which includes class 1, 2, 3 markers.

Class 2 MHC markers are also called HLA-Dr. There are a lot of autoimmune diseases which are connected with genetic disturbances of HLA-Dr system. That is why HLA genes are included into predisposing factors in the pathogenesis of autoimmune diseases.

In the pathogenesis of autoimmune diseases the following factors are distinguished:

• predisposing (HLA genes, hormonal background, genetically dependent features of the target cells);

• initiating (viral and bacterial infections, exposure of immune system and target organs to chemical and physical factors);

• contributing (dysfunction of immune system, T-lymphocyte suppressor activity).

In the pathogenesis, 2 mechanisms can be distinguished, therefore all the autoimmune diseases can be divided into 2 groups.

Group 1. Organ specific diseases. They are characterized by disturbance of physiological isolation of the organs and tissues due to absence of immune tolerance. Lymphohistiocyte infiltration occurs in the tissues (like at slow hypersensitivity reaction). The main organ specific diseases are:

1. Endocrine glands: Hashimoto's (autoimmune) thyroiditis. Graves' disease.

Insulin-dependent diabetes mellitus. Idiopathic Addison's disease.

2. Alimentary tract:

Autoimmune atrophic gastritis in pernicious anemia.

Ulcerative colitis. Crohn's disease.

3. Blood cells:

Autoimmune hemolytic anemia. Autoimmune thrombocytopenia.

4. Others:

Myasthenia gravis.

Autoimmune orchitis.

Autoimmune encephalomyelitis.

Goodpasture's syndrome.

Primary biliary cirrhosis.

Chronic active hepatitis.

Membranous glomerulonephritis.

Autoimmune skin diseases.

Group 2. Organ non-specific diseases. Primary disturbances in the immune system causing the loss of ability to distinguish «own» and «foreign» antigens. They are:

Systemic lupus erythematosus.

Rheumatoid arthritis.

Scleroderma (Progressive systemic sclerosis).


Polyarteritis nodosa (PAN).

Sjogren's syndrome.

Reiter's syndrome.

Mixed connective tissue disease.

The diseases with autoimmune disturbances.

In these diseases antigenic properties of the tissues change, which causes immune reaction development.

Autoimmunization is responsible not for the beginning but the progress of the disease as autoimmune antibodies appear during the disease. It is observed in glomerulonephritis, hepatitis, chronic gastritis, burn disease, rheumatism, liver cirrhosis.

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