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Long-Term Commitment to Inflammation-Seeking Homing in CD4⁺ Effector Cells¹

Silke Jennrich^*, Boris A. Ratsch^*, Alf Hamann^* and Uta Syrbe^2,*,

^* Charité, Campus Mitte, Experimentelle Rheumatologie, c/o Deutsches Rheumaforschungszentrum, Berlin, Germany; and Charité, Campus Benjamin Franklin, Medizinische Klinik I, Germany

Access of T effector cells to sites of inflammation is a prerequisite for an efficient action in immune defense and is mediated by different, partly tissue-specific sets of adhesion molecules. To what extent lymphocytes memorize the site of initial priming and develop organ-specific homing properties is still a matter of debate. Notably, data on the stability of homing receptor expression on T cells in vivo are largely lacking. We approached this question by the adoptive transfer of CD4⁺ T cells sorted for the expression of P-selectin ligands, which contribute to migration into inflamed sites in skin and other tissues. We observed long-term expression of P-selectin ligands on roughly one-third of effector cells. On those cells that had lost P-selectin ligands, re-expression upon Ag challenge was observed but only within pLNs, similar to the organ-selective induction upon the primary activation of naive T cells. The frequency of cells stably expressing P-selectin ligands was higher when cells were repeatedly stimulated under permissive conditions in the presence of IL-12, indicating a gradual fixation of this phenotype. In line with that finding, isolated P-selectin ligand positive memory T cells showed the highest frequency of long-term expressing cells. A tissue-specific environment was not required for the long-term maintenance of P-selectin ligand expression on the subfraction of effector cells. These data indicate that the expression of selectin ligands can become clonally imprinted under certain conditions, but also that a major fraction of the cells remains flexible and subject to environmental modulation upon restimulation.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Deutsche Forschungsgemeinschaft Grants SFB 366 C7 and SY31/2-1.

² Address correspondence and reprint requests to Dr. Uta Syrbe, Charité, Campus Benjamin Franklin, Medizinische Klinik I, 12200 Berlin, Germany. E-mail address: uta.syrbe{at}charite.de

³ Abbreviations used in this paper: P-lig, P-selectin ligand; E-lig, E-selectin ligand; mLN, mesenteric lymph node; OVAtg, OVA TCR transgenic; pLN, peripheral lymph node.