44. Immunopathology. Autoimmune reactions and diseases. Role of hypersensitivity reactions (rapid and delayed reactions) in autoimmune diseases · Microbiology · MU Sofia

Immunopathology. Autoimmune reactions and diseases. Role of hypersensitivity reactions (rapid and delayed reactions) in autoimmune diseases. Immunodeficiency. Immunopathology

Immunopathology involves pathological immune responses that lead to disease.
It occurs when the immune system is inadequate, inappropriate, or misdirected.
This often results in tissue damage.
Immunopathology includes hypersensitivity disorders, immune deficiency diseases, and autoimmune diseases.
Clinical symptoms of infections can arise from excessive host immune responses. Immune reactions can both protect and potentially damage host health.
Cellular immunopathology results from excessive T-cell responses against low cytopathogenicity infections or allogenic organ transplants.

Autoimmunity is the immune system's ability to identify its own healthy cells.
Autoimmune diseases are caused by the immune system's inability to differentiate between self- and non-self antigens.
In these diseases, the immune system destroys healthy cells.

Autoimmune diseases stem from a failure of tolerance.
Self-tolerance is the mechanism by which the immune system learns not to react to self-antigens.
Mechanisms like central tolerance (elimination of self-reactive T/B cells in thymus/bone marrow) and peripheral tolerance (deletion or inactivation of autoreactive cells escaping central elimination) delete or inactivate self-reactive cells or suppress destructive responses. Loss of these mechanisms impairs self-tolerance, causing autoimmune disease.
Autoimmunity can be tissue/organ specific (e.g., Type 1 Diabetes, Graves' disease, Myasthenia gravis) or systemic (e.g., Rheumatoid arthritis, Systemic lupus).
Triggers may include environmental stimuli like infections (bacterial or viral).
Molecular mimicry, where microbial antigens resemble self-antigens, can lead to the immune system attacking host tissues (e.g., rheumatic fever).
Release of sequestered self-antigens (normally hidden from the immune system) can cause them to be seen as foreign.
Examples of autoimmune diseases include Systemic lupus erythematosus (SLE), Rheumatoid arthritis (RA), Graves' disease, Multiple sclerosis (MS), and Type 1 diabetes.

Hypersensitivity reactions contribute to autoimmune diseases.
Specific types are involved:
Type II (Antibody-Mediated/Cytotoxic): Involves IgM and IgG autoantibodies binding to cell surface or extracellular matrix antigens. This leads to cell damage via complement or inflammatory cells or interferes with receptor function.
Examples: Antibodies against acetylcholine receptors in Myasthenia gravis disrupt neuromuscular transmission. Antibodies stimulating the TSH receptor in Graves' disease cause excessive thyroid hormone production.
Type III (Immune Complex Mediated): Involves IgG autoantibodies binding to soluble self-antigens, forming immune complexes. These complexes deposit in tissues (like vessel walls, joints, kidney), activating complement and causing inflammation and tissue damage.
Examples: Deposition in kidneys, skin, and joints in Systemic lupus erythematosus (SLE) causes systemic inflammation. Immune complexes in joints contribute to chronic damage in Rheumatoid arthritis.