Lecture 3_ Autoimmunity_pt1

A: Paul Ehrlich coined it in the 1900s; it means “fear of self-poisoning.”

A: Autoimmune diseases.

A: Immune responses are targeted toward self-antigens, causing damage to organs and tissues in the body.

A: They can be T cell–mediated or due to antibodies (Abs) against host antigens (Ags).

A: More than 100.

A: Yes, they can involve various organ systems.

A: Chronic illness and death.

A: About 5%.

A: More than 20 million.

A: The ability of the immune system to discriminate “self” from “non-self” or “foreign,” showing unresponsiveness to self antigens (Ags).

A: Lymphocytes must be “educated” at two levels (layers of protection) during development or immune response.

A: Self-reactive immature T cells and B cells are deleted, change their specificity (B cells only), or (in the case of CD4+ T cells) develop into Treg cells.

A: Self-reactive mature T cells or B cells in the peripheral tissues may be inactivated or suppressed by regulatory T cells.

central tolerance vs peripheral tolerance

T cell central tolerance

T cell central tolerance

T-cell peripheral tolerance

B-cell central tolerance

B-cell peripheral tolerance

A: Autoimmune diseases are more prevalent among family members and more common in monozygotic (genetically identical) twins than dizygotic (non-identical) twins or siblings.

A: MHC genes.

A: People inheriting the HLA-B27 allele are at 100 times higher risk of developing ankylosing spondylitis.

A: Polymorphism in non-MHC genes.

A: IL2RA gene, which is involved in T-cell activation and maintenance of Tregs.

A: Around 20–30 genes.

A: Endogenous and environmental factors.

A: Women. >:(

A: Estrogens promote Th2 response (more B-cell activation and antibody production), while androgens promote Th1 response with activation of CD8+ T cells.

A: Tissue damage caused by infections, toxins, or injury.

A:

Autoantibodies to the lens of the eye after ocular injury

Autoantibodies to sperm after vasectomy

Autoantibodies to DNA or skin cells after UV damage

A: Exposure to environmental toxins, ingestion of harmful foods or drugs, or the aging process.

A: They make self-antigens more immunogenic.

A: Citrullination of collagen may play a role in rheumatoid arthritis (RA), and glycosylation of myelin may be involved in multiple sclerosis (MS).

A: Molecular mimicry.

A: Exposure to viral or bacterial antigens may trigger immune responses that cross-react with similar self-antigens.

A: The association between Streptococcus pyogenes and rheumatic fever, which affects the joints and heart.

A: Complex interactions between genetic and environmental factors.

A: Female hormones, tissue injury and release of self-antigens, microbial infections, and epigenetic factors (toxins, foods, drugs, aging, post-translational modifications).

A: Possession of certain HLA or other genes.

A: Activation of self-reactive T cells and B cells and development of immune responses to self-antigens.

A: Development of autoimmune disease.