Undesired meeting of lymphocytes: organ-specific infiltration and the organization of ectopic lymphoid tissue in a murine experimental autoimmune gastritis.

Autoimmune diseases are caused by the misdirected attack of the immune system against the body's own components. Delicate balance between the activities of several CD4+ T cell subsets is crucial for determining the initiation of autoimmunity and disease state. In addition, complicated interactions between immune effector cells and tissue resident cells take place in the target organ and construct the inflammatory microenvironment. During the acute/deterioration phase, autoreactive and cytotoxic effector cells leave blood vessels to infiltrate the target site through a multi-step mechanism involving various molecular processes, and disease pathology progresses though a vicious cycle of accumulation and activation of effector cells. In the chronic phase, long-lasting infiltration of activated lymphocytes in the focal site occasionally results in the formation of ectopic lymphoid tissue that possibly plays important roles in sustaining self-reactivity. The murine experimental model of autoimmune gastritis is one of the most useful systems for studying the complicated cellular events associated with chronic inflammatory disease.