Inflammatory response, interferons, and phagocytes

Response with B and T lymphocytes

Inflammatory response

Intact skin and mucous membranes, and phagocytes

Complement proteins, cilia, and gastric juices

tonsillar corpuscles

tonsillar crypts

germinal centers

lymphoid follicles

Inflammation increases capillary permeability.

Release of prostaglandins results in pain.

Vasoconstriction prevents excessive blood loss due to injury.

Chemotaxis draws leucocytes to the site of injury.

Uncontrolled cell division resulting in cell surface abnormalities recognized by NK cells.

Infection and death of T helper cells by a virus, resulting in a loss of adaptive immunity.

Antibody binding to acetylcholine receptors of the motor end plate resulting in muscle weakness.

Release of bacterial endotoxins that block acetylcholine release and result in muscle paralysis

that do not recognize self-M H C proteins undergo apoptosis

that contain MHC receptors undergo apoptosis

that do not recognize self-antigens displayed on self-MHC proteins undergo apoptosis

that demonstrate immunological self-tolerance undergo apoptosis