CD8+ αβ+ T Cells That Lack Surface CD5 Antigen Expression Are a Major Lymphotactin (XCL1) Source in Peripheral Blood Lymphocytes

Laura Stievano, Valeria Tosello, Novella Marcato, Antonio Rosato, Annalisa Sebelin, Luigi Chieco-Bianchi, Alberto Amadori

Research output: Contribution to journalArticlepeer-review

Abstract

To better characterize the cellular source of lymphotactin (XCL1), we compared XCL1 expression in different lymphocyte subsets by real-time PCR. XCL1 was constitutively expressed in both PBMC and CD4+ cells, but its expression was almost 2 log higher in CD8+ cells. In vitro activation was associated with a substantial increase in XCL1 expression in both PBMC and CD8+ cells, but not in CD4+ lymphocytes. The preferential expression of XCL1 in CD8+ cells was confirmed by measuring XCL1 production in culture supernatants, and a good correlation was found between figures obtained by real-time PCR and XCL1 contents. XCL1 expression was mostly confined to a CD3+CD8+ subset not expressing CD5, where XCL1 expression equaled that shown by γδ + T cells. Compared with the CD5+ counterpart, CD3 +CD8+CD5- cells, which did not express CD5 following in vitro activation, showed preferential expression of the αα form of CD8 and a lower expression of molecules associated with a noncommitted/naive phenotype, such as CD62L. CD3+CD8 +CD5- cells also expressed higher levels of the XCL1 receptor; in addition, although not differing from CD3+CD8 +CD5+ cells in terms of the expression of most α- and β-chemokines, they showed higher expression of CCL3/macrophage inflammatory protein-1α. These data show that TCR αβ -expressing lymphocytes that lack CD5 expression are a major XCL1 source, and that the contribution to its synthesis by different TCR αβ -expressing T cell subsets, namely CD4+ lymphocytes, is negligible. In addition, they point to the CD3+CD8+CD5- population as a particular T cell subset within the CD8+ compartment, whose functional properties deserve further attention.

Original languageEnglish
Pages (from-to)4528-4538
Number of pages11
JournalJournal of Immunology
Volume171
Issue number9
Publication statusPublished - Oct 1 2003

ASJC Scopus subject areas

  • Immunology

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