autoimmune diseases Flashcards
etiology of autoimmune diseases
genetic disposition - HLA polymorphism
hormonal influences (more women)
enviromental factors: medications, stress, other diseases
reasons for autoimmune
expression of co-stimulatory molecules and the presentation of pathogen and self-antigens through IFN-gamma
failure of apoptosis
polyclonal lymph activation
exposure of cryptic antigens
antibody mediated cytotoxicity
type 2 hypersensitivity (ADCC, CDC, opsonization and phagocytoses) good pastures syndrome (antibody attack on basement membrane)
autoimmune-complex disease
vasculature, join and glomeruli (complement, phagocytosis, inflammation) type 3 hypersensitivity
arthritis, vasculitis
cell-mediated autoimmne
cytotoxic T cells react with self-antigen resulting in specific tissue destruction (T1D- inflammatory cytokine in type 1 diabetes, whole B cell population is wiped out and can’t secrete insulin
autoimmune hemolytic anemia
type 2 hyposensitivity, autoantibodies against RBC, lead to hemolysis
goodpasture’s syndrome
autoantibodies against glomerular basement membrane, collagen type IV, leading to progressive gomerulonephritis
acute rheumatic fever
strep cell wall antibodies cross-reacting with cardiac muscle, leading to arthritis and myocarditis
immune thrombocytopenic purpura
autoantibodies against platelet GPIIb-IIIa (2 adhesion antibodies), leading to low platelet count and bleeding - bruise easily
Myesthenia Gravis
autoantibodies against the ach receptor on the motor end plates of the muscle, leading to complement-dependent damage to the receptor, skeletal muscle weakness - drop eyelids
graves disease
autoantibodies act as agonists of TSH, leading to hyperthyroidism
RA
systemic but principally joint inflammation rheumatoid factors (autoantiboides against IgG Fc) in the serum and synovium, lymph and macrophage infiltration, TNF- alpha and other inflammatory cytokines
essential mixed cryoglobulinemia
rheumatoid factor (IgG/IgM)-IgG complexes leading to systemic vasculitis (not in joint, inverse)
systemic lupus erythematosus (SLE)
immune complexes formed with nuclear components (DNA, histones, etc) rash, arthritis, glomerulonephritis, vasculitis
type 1 diabetes mellitus
pancreatic b-cell autoantigens, b-cell destruction, insulin-dependent