Lymphocyte homing receptor

Lymphocyte homing receptors are

High endothelial venules (HEVs) are cells found in secondary lymphoid organs that express large quantities of cell adhesion molecules, enabling undifferentiated lymphocytes to bind.^[2] After entering lymph nodes and Peyer’s patches via HEVs, naive T and B cells are exposed to antigen circulating in lymph and differentiate to contribute to the adaptive immune response. HEVs develop from cytokine production after exposure to antigen and express adhesion molecules from the selectin family, mucin-like family, and the Ig superfamily.^[5] Naive lymphocyte extravasation into Peyer’s patches is often mediated by L-selectin and limited expression of α4 integrins and other homing receptors prevents these lymphocytes from accessing mucosal effector tissue.^[4]

Mature lymphocyte homing

Mature lymphocytes are constantly recirculating in the blood and can traffic to secondary lymphoid tissue as well as target tissue including mucosal tissues of the lamina propria, inflammation, and other extralymphoid immune effector sites. Lymphocyte homing receptor expression is altered by antigen exposure. This function enables the adaptive immune system to specialize an immune response in different parts of the body.^[4]

Upon exposure to antigens, lymphocytes lack homing ability during a period of sessile differentiation and cell division, and antigen specific lymphocytes are stored in the spleen for 1–3 days. Subsequently, antigen-stimulated B and T cells express homing receptors particularly for the HEV in initial site of immunization tissue.^[2] Furthermore, lymphocytes can alter cell adhesion molecule “activatability” to increase binding ability.^[4] Organ-specific lymphocyte homing is important for antigen-specificity and in avoiding autoimmune cross-reactions.^[2]

Extravasation of lymphocytes

Lymphocyte homing occurs in four steps leading to extravasation into target tissue; Rolling, activation, activation-dependent “arrest”, and