Figure 1. Trafficking of naive and effector CD8 T cells.

(A) Naive CD8 T cells enter lymph nodes through the high endothelial venule. Rolling and tethering is mediated by interactions between L-selectin (CD62L) and PNAd, which allows the chemokine receptor CCR7 to interact with CCL19 or CCL21 displayed by the endothelial cells. CCR7 ligation results in polarization and activation of the integrin LFA-1, which will bind to its ligand ICAM-1 and cause the naive CD8 T cell to firmly adhere to the surface of the high endothelial venule before transmigrating across the endothelial layer. (B) Following antigenic stimulation, effector CD8 T cells express functional ligands such as PSGL-1 and CD44, that bind P-selectin and E-selectin expressed by inflamed tissues. Effector T cells also express chemokine receptors (such as CXCR3), which interact with inflammatory chemokines (such as CXCL10) that are produced by the inflamed tissues. This causes activation and polarization of LFA-1 on the effector T cell, as well as newly expressed integrins, such as VLA-4, which will bind to ICAM-1 and VCAM-1 on the inflamed tissue, respectively. These interactions result in firm adhesion, allowing the effector CD8 T cell to then transmigrate through the endothelial layer and into the inflamed tissue.

LFA: Lymphocyte function-associated antigen; PNAd: Peripheral node addressin; PSGL: P-selectin glycoprotein ligand; VLA: Very-late antigen.