A1 Refereed original research article in a scientific journal
Ly6C supports preferential homing of central memory CD8(+) T cells into lymph nodes
Authors: Hanninen A, Maksimow M, Alam C, Morgan DJ, Jalkanen S
Publisher: WILEY-BLACKWELL
Publication year: 2011
Journal: European Journal of Immunology
Journal name in source: EUROPEAN JOURNAL OF IMMUNOLOGY
Journal acronym: EUR J IMMUNOL
Number in series: 3
Volume: 41
Issue: 3
First page : 634
Last page: 644
Number of pages: 11
ISSN: 0014-2980
DOI: https://doi.org/10.1002/eji.201040760
Abstract
Ly6C is a murine cell-surface antigen expressed by plasma cells, subsets of myeloid cells and many T cells, including memory T cells. We previously documented that Ly6C crosslinking induces LFA-1 clustering on naive CD8 1 T cells. Here, we show that in vitro and in vivo differentiation of naive CD8 1 T cells into central (Tcm) but not effector (Tem) memory T cells enhances Ly6C expression, and its crosslinking induces strong LFA-1 clustering on Tcm. Blocking Ly6C function inhibits in vivo Tcm homing to LNs as efficiently as blocking L-selectin but it does not potentiate the inhibition provided by blocking either L-selectin or LFA-1 function. Thus, Ly6C, L-selectin and LFA-1 all appear to be part of a common homing pathway. In vitro, Ly6C crosslinking enhances Tcm adherence to ICAM-1 in the presence of CCL21. In summary, Tcm homing involves Ly6C, in addition to L-selectin and LFA-1, and appears to potentiate firm adhesion of Tcm to ICAM-1 in synergy with a chemokine. We propose that Ly6C augments Tcm compartmentalization into LNs during their homing.
Ly6C is a murine cell-surface antigen expressed by plasma cells, subsets of myeloid cells and many T cells, including memory T cells. We previously documented that Ly6C crosslinking induces LFA-1 clustering on naive CD8 1 T cells. Here, we show that in vitro and in vivo differentiation of naive CD8 1 T cells into central (Tcm) but not effector (Tem) memory T cells enhances Ly6C expression, and its crosslinking induces strong LFA-1 clustering on Tcm. Blocking Ly6C function inhibits in vivo Tcm homing to LNs as efficiently as blocking L-selectin but it does not potentiate the inhibition provided by blocking either L-selectin or LFA-1 function. Thus, Ly6C, L-selectin and LFA-1 all appear to be part of a common homing pathway. In vitro, Ly6C crosslinking enhances Tcm adherence to ICAM-1 in the presence of CCL21. In summary, Tcm homing involves Ly6C, in addition to L-selectin and LFA-1, and appears to potentiate firm adhesion of Tcm to ICAM-1 in synergy with a chemokine. We propose that Ly6C augments Tcm compartmentalization into LNs during their homing.
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