![]() Similarly, after Candida albicans infection, mouse skin was shown to harbor both resident and migratory CD4 memory T cells ( Park et al., 2018). In support of recirculation, CD4 + T cells expressing intermediate levels of CCR7 and CD62L have been shown to egress from the skin of specific pathogen–free (SPF) mice ( Bromley et al., 2013). In humans, alemtuzumab (anti-CD52) depletes circulating cells, but leaves behind CCR7 − CD4 + T cells in skin, supporting that they are resident. However, CD62L +/CCR7 + (central memory T cell ) and CD62L −/CCR7 + (migratory memory T cell) CD4 + T cells are depleted, indicating skin recirculation ( Watanabe et al., 2015). In a separate study, CD4 + T cells that confer protective immunity against Leishmania major were shown to be resident by skin grafting experiments ( Glennie et al., 2015). While skin surveillance by memory CD8 + T cells appears dominated by residence, memory CD4 + T cell immunosurveillance may be more complex. Many T RM stably express CD69, and most memory CD4 + and CD8 + T cells isolated from lymphoid or NLTs of human cadavers express CD69 ( Sathaliyawala et al., 2013 Thome et al., 2014). However, reports in non-SPF mice indicate that CD69 expression may not be sufficient to infer residence ( Beura et al., 2018). Indeed, residence can be difficult to quantify. First, there are no perfect markers unequivocal evaluation really still depends on migration experiments, and experimental approaches have varied considerably.
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