Autoimmunity + Inflammation Complete

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What is inflammation?

Protective response to infection, injury or tissue damage that eliminates the cause and initiates repair.

Five cardinal signs of inflammation?

Redness, heat, swelling, pain and loss of function.

Difference between acute and chronic inflammation?

Acute: rapid, neutrophils, days. Chronic: prolonged, macrophages/lymphocytes, tissue destruction and fibrosis.

What triggers inflammation?

PAMPs and DAMPs detected by pattern-recognition receptors.

Major cells initiating inflammation?

Macrophages, dendritic cells and mast cells.

Key pro-inflammatory cytokines?

TNF-α, IL-1 and IL-6.

Main function of chemokines?

Recruit leukocytes to the site of injury.

Role of histamine?

Vasodilation and increased vascular permeability.

Role of prostaglandins?

Pain, fever and vasodilation.

Role of complement?

Opsonisation, chemotaxis and pathogen lysis.

Steps of phagocytosis?

Recognition → engulfment → phagosome → phagolysosome → destruction.

Main phagocytic cells?

Neutrophils and macrophages.

What is opsonisation?

Coating pathogens to enhance phagocytosis.

What is resolution of inflammation?

Removal of stimulus followed by tissue repair and return to homeostasis.

What is fibrosis?

Excess collagen deposition causing scar tissue.

Definition of autoimmunity?

Immune response directed against self-antigens.

What is self-tolerance?

Ability of the immune system to avoid attacking self-tissues.

Central vs peripheral tolerance?

Central occurs in thymus/bone marrow; peripheral suppresses self-reactive cells that escape.

Genetic factors in autoimmunity?

HLA variants increase susceptibility.

Environmental triggers of autoimmunity?

Infections, smoking, UV light and drugs.

Mechanism leading to autoimmune disease?

Genetic susceptibility + environmental trigger → loss of self-tolerance → autoantibodies/T cells → tissue damage.

Type 1 hypersensitivity mediator?

IgE and mast cells.

Type 2 hypersensitivity mechanism?

IgG/IgM antibodies against cell surface antigens.

Type 3 hypersensitivity mechanism?

Immune complex deposition causing inflammation.

Type 4 hypersensitivity mechanism?

T-cell mediated delayed hypersensitivity.

Rheumatoid arthritis pathogenesis?

Autoimmune synovial inflammation causing pannus formation, cartilage destruction and bone erosion.

Key autoantibodies in rheumatoid arthritis?

Rheumatoid factor and anti-CCP antibodies.

Osteoarthritis vs rheumatoid arthritis?

OA is degenerative; RA is autoimmune inflammatory.

Systemic lupus erythematosus mechanism?

Autoantibodies form immune complexes that deposit in tissues.

What are granulomas?

Organised collections of macrophages in chronic inflammation.

IL-1 and TNF-α systemic effects?

Fever, increased vascular permeability and acute phase response.

Clinical features of chronic inflammation?

Persistent inflammation, macrophages, lymphocytes, fibrosis and tissue destruction.