The immune system operates through innate (nonspecific) and adaptive (specific) defense mechanisms that protect against pathogens while maintaining self-tolerance. Autoimmune diseases arise when immune tolerance breaks down, leading to self-reactive T cells and B cells that target host tissues — molecular mimicry, epitope spreading, and genetic susceptibility (HLA associations) contribute to autoimmune pathogenesis. Type I hypersensitivity (anaphylaxis) involves IgE-mediated mast cell degranulation releasing histamine, leukotrienes, and prostaglandins, causing vasodilation, bronchospasm, and increased vascular permeability. Immunodeficiency states, whether primary (genetic) or secondary (HIV, immunosuppressive therapy), increase susceptibility to opportunistic infections and malignancies.