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Original Article

^a The Center for Blood Research, Harvard Medical School, Boston, MA 02115
^b Department of Pathology, Harvard Medical School, Boston, MA 02115
^c Department of Pediatrics, Harvard Medical School, Boston, MA 02115
The Center for Blood Research, 200 Longwood Ave., Boston, MA 02115.617-278-3190617- 278-3130

uva{at}cbr.med.harvard.edu

It has been proposed that two different antigen-experienced T cell subsets may be distinguishable by their preferential ability to home to lymphoid organs (central memory cells) or nonlymphoid tissues (effector memory/effector cells). We have shown recently that murine antigen-primed CD8⁺ T cells cultured in interleukin (IL)-15 (CD8^IL-15) resemble central memory cells in phenotype and function. In contrast, primed CD8⁺ T cells cultured in IL-2 (CD8^IL-2) become cytotoxic effector cells. Here, the migratory behavior of these two subsets was investigated. Naive, CD8^IL-15 cells and, to a lesser degree, CD8^IL-2 cells localized to T cell areas in the spleen, but only naive and CD8^IL-15 cells homed to lymph nodes (LNs) and Peyer's patches. Intravital microscopy of peripheral LNs revealed that CD8^IL-15 cells, but not CD8^IL-2 cells, rolled and arrested in high endothelial venules (HEVs). Migration of CD8^IL-15 cells to LNs depended on L-selectin and required chemokines that bind CC chemokine receptor (CCR)7. Both antigen-experienced populations, but not naive T cells, responded to inflammatory chemokines and accumulated at sites of inflammation. However, CD8^IL-2 cells were 12 times more efficient in migrating to inflamed peritoneum than CD8^IL-15 cells. Furthermore, CD8^IL-15 cells proliferated rapidly upon reencounter with antigen at sites of inflammation. Thus, central memory-like CD8^IL-15 cells home avidly to lymphoid organs and moderately to sites of inflammation, where they mediate rapid recall responses, whereas CD8^IL-2 effector T cells accumulate in inflamed tissues, but are excluded from most lymphoid organs.

Key Words: lymphocyte homing • lymph node • chemokines • adhesion molecules • inflammation

© 2001 The Rockefeller University Press

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