Abstract
Over the last several years, a number of papers have called attention to a distinct population of γδ T cells preferentially found in the dermis of the skin of normal mice. These cells appear to play an important role in promoting the development of psoriasis, but also are critical for host resistance to particular pathogens. They are characterized by the expression of a limited subset of γδ T cell receptors and a strong propensity to secrete IL-17. Perhaps most importantly, humans appear to carry an equivalent dermal γδ T cell population, likewise biased to secrete IL-17 and also implicated as playing a pathogenic role in psoriasis. This review will attempt to summarize and reconcile recent findings concerning the dermal γδ T cells.
Highlights
Over the last several years, a number of papers have called attention to a distinct population of γδ T cells preferentially found in the dermis of the skin of normal mice
One of the earliest examples of this was the discovery that most T cells present in the epidermis of mice, known as dendritic epidermal T cells (DETC), are γδ T cells expressing identical T cell receptors (TCRs), composed of Vγ5- and Vδ1-containing TCR chains that carry identical or nearly identical junctional sequences [1]
Upon examining the T cells present in the draining lymph nodes of mice with collagen-induced arthritis, we found a preferential increase in γδ T cells expressing a Vγ4Vδ4 TCR, and showing a strong bias to secrete IL-17A
Summary
One of the first characteristics of γδ T cells that distinguished them from classical αβ T cells was their relative abundance in certain anatomical sites, in epithelial tissues. Though the reason for a need for a particular T cell type in the epidermis having a predetermined specificity is still not understood, in the last few years it has become clear that another skin-associated γδ T cell population exists, residing in the dermis rather than epidermis The existence of these cells was first suggested by a finding from our laboratory in a study involving mice with collagen-induced arthritis. A more in-depth analysis revealed that these cells express nearly invariant TCR junctions [5], which could either suggest the oligoclonal expansion of γδ T cells having a certain specificity, or that the cells represent, like DETC, a fetal-derived subset This strong response by Vγ4Vδ4+ γδ cells was not dependent upon the mice developing arthritis, required CFA but not collagen in the immunizing inoculum [5], and depended upon immunization via the skin, by intradermal or subcutaneous inoculation, which we confirmed in a later study [6]. The production of IL-17y these γδ T cells, which was elicited by culture with IL-23, required the presence of both γδ and αβ T cells, and the ability of the two cell types to make physical contact [8]
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