The CD7− T cell subset represents the majority of IL-5-secreting cells within CD4+CD45RA− T cells

Abstract

SUMMARYAbsence of CD7 is a stable phenotype in a subset of normal human T cells. Most circulating CD7 ÿ T cells express the CD4CD45RO CD45RA ÿ memory phenotype. We analysed CD4 CD45RA ÿ peripheral blood lymphocytes that were separated into CD7 and CD7 ÿ for their in vitro cytokine secretion in response to different stimuli. The CD4 + CD7 -subpopulation was found to secrete significantly higher levels of IL-5 compared with the CD4 + CD7 + subset upon stimulation with ionomycin/phorbol myristate acetate (PMA) plus anti-CD28 MoAbs. In contrast to IL-5 secretion, IL-4 and interferon-gamma (IFN-°) secretion was not significantly different in CD7 and CD7 ÿ T cells upon stimulation in vitro. The data indicate that the CD4 CD7 ÿ T cell represents the majority of IL-5-secreting cells within the population of CD4 CD45RA ÿ memory T cells. Since CD4 CD7 ÿ T cells were found to be enriched in various skin lesions associated with eosinophilic infiltration, the results of our study support the hypothesis that skin-infiltrating CD7 ÿ T cells are one of the major sources of IL-5 responsible for the development of eosinophilic inflammation in certain skin diseases.

Accumulation of CD4+CD7− T cells in inflammatory skin lesions: evidence for preferential adhesion to vascular endothelial cells

“…Our model is supported by the finding that CLA-enriched memory T cells migrated more actively across cytokine-activated EC than CLA-depleted memory T cells [33]. Furthermore, cells of the CD4 1 CD7 2 subset secrete cytokines with a Th0/Th2-like profile [12] and represent the majority of IL-5-secreting cells within the population of CD4 1 CD45RA 2 memory T cells in vitro [34]. Most chronic inflammatory skin diseases are associated with local accumulation of tissue eosinophils, and local damage caused by eosinophilderived products is believed to contribute to the pathogenesis of these diseases [35].…”

The CD7− subset of CD4+ memory T cells is prone to accelerated apoptosis that is prevented by interleukin-15 (IL-15)

“…This T-cell subset, moreover, contributes by secretion of IL-5, in addition to IL-4 and IFN-g, to attract an eosinophilic infiltrate 50,51 that on their part is believed to play a substantial role in epithelial cell damage by eosinophil-derived products. This mechanism fits well with the observation that skin infiltrating CD4 + CD7 7 T cells accumulate within the chronic inflammatory lesion, a site with locally high concentrations of TNF-a and with eosinophilic infiltrates.…”

CD7−T Cells are Late Memory Cells Generated from CD7+T Cells

“…These cells are, however, not anergic as they secrete a distinct panel of cytokines in increased levels, including IL-4 and IL-5, upon appropriate stimulation. 4 It is noteworthy that CD7 Ϫ T cells express receptors associated with homing to the skin, including cutaneous lymphocyte antigen (CLA), 5 and are resistant to apoptosis induced by the CD7 ligand galectin-1, a lectin ubiquitously expressed in connective tissues, whereas CD7 ϩ T cells enter apoptosis upon galectin-1 binding. 6 CD4 ϩ CD7 Ϫ T cells, in contrast to CD4 ϩ CD7 ϩ T cells, increase in numbers in the peripheral blood during certain physiologic and pathologic conditions in vivo.…”