81. Stimulation of the cellular link of immunity: participants in immunity, causes. Pathological anatomy of changes in the organs of the immune system (in the lymph nodes, spleen, bone marrow, thymus).

Cellular immune response:

• It is provided by the reaction of T-killers, NK cells and activated macrophages with cytotoxic effects.

• Auxiliary cells such as T-helper cells and APC are also involved in the response.

Conditions for triggering the cellular immune response (differentiation of Th0 into Th1)

1. The viral, tumor, or transplant nature of hypertension,

2. High or low density of AG on the agroindustrial complex,

3. Presentation of AG by a dendritic cell or macrophage,

4. Microenvironment characteristic of lymph nodes,

5. Cytokines IL-2, IL-12, IFNu.

Depending on the localization of pathogens inside the cell, there are 2 variants of the cellular immune response:

• Cytotoxic cellular immune response.

• The pathogen is localized in the cytosol of the cell: – viruses, – transplant antigens.

• Inflammatory cellular immune response.

• The pathogen is localized in granules:

–bacteria-intracellular parasites (chlamydia, Leishmania, rickettsia, mycobacteria),

– protozoa (Leishmania),

– mushrooms (candida).

Pathology of the immune system:

1. Hypersensitivity reactions, I-VI

2. "Autoimmune" diseases, i.e. "collagen diseases"

3. Immunodeficiency syndromes:

-primary (genetic)

-secondary (purchased)

4. Immunoproliferative tumor diseases – lymphomas

82. Hypersensitivity reactions: definition of the concept, classification according to Coombs. Pathological anatomy of type I hypersensitivity reaction , mechanism and scheme of the reaction, examples of diseases.

HYPERSENSITIVITY REACTIONS

1. IMMEDIATE TYPE (IG E)

2. ANTIBODY MEDIATED

3. IMMUNOCOMPLEX

4. CELL-MEDIATED (DELAYED TYPE).

Type I hypersensitivity (diseases):

• Bronchial asthma (atopic forms)

• Anaphylactic shock

• Urticaria

• Quincke's edema

• Food allergies

• Allergic rhinitis

• Allergic conjunctivitis

Type I hypersensitivity:

The reaction rate is seconds to minutes

IgE (reagin antibodies) are mediated

Chemical mediators of damage - vasoactive products of mast cells/basophils (histamine, arachidonic acid derivatives, serotonin,)

The mechanism is fullness of blood, spasm of smooth muscles. Hypersecretion of viscous mucus, accumulation of neutrophils, eosinophils, mast cells.

Reaction scheme:

1. Contact with the allergen.

2. Synthesis of IgE.

3. Fixation of IgE on the surface of mast cells (Sensitization phase)

4. Repeated contact with the same allergen, or antigens that share epitopes with allergens.

5. Binding of the antigen to IdE on the surface of mast cells and basophils (Activation phase)

6. Release of mediators from mast cells, basophils, eosinophils

7. The effect of these mediators on organs and tissues (Effector phase)

83. II hypersensitivity reaction , mechanism and scheme of the reaction, examples of diseases.

Secreted antibodies are directly involved in cell damage, followed by phagocytosis or lysis (with or without complement) and tissue damage by associated inflammation.

Antibodies can also disrupt tissue function and cause diseases without tissue damage (acting on hormone receptors such as thyroid or acetylcholine)

Diseases: autoimmune hemolytic anemia, transfusion of foreign blood, hemolytic disease of the fetus and newborn, Goodpasture syndrome, autoimmune thyroiditis, myasthenia gravis, bullous pemphigoid

The production of Ig, M, which are attached to the antigen of target cells, followed by phagocytosis or lysis by their activated complementary Fc receptors and exit. leukocytes.

Pathological changes - cell lysis, inflammation.