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Tumor-induced MDSC act via remote control to inhibit L-selectin-dependent adaptive immunity in lymph nodes #MMPMID27929373
Ku AW; Muhitch JB; Powers CA; Diehl M; Kim M; Fisher DT; Sharda AP; Clements VK; O'Loughlin K; Minderman H; Messmer MN; Ma J; Skitzki JJ; Steeber DA; Walcheck B; Ostrand-Rosenberg S; Abrams SI; Evans SS
Elife 2016[Dec]; 5 (?): ? PMID27929373show ga
Myeloid-derived suppressor cells (MDSC) contribute to an immunosuppressive network that drives cancer escape by disabling T cell adaptive immunity. The prevailing view is that MDSC-mediated immunosuppression is restricted to tissues where MDSC co-mingle with T cells. Here we show that splenic or, unexpectedly, blood-borne MDSC execute far-reaching immune suppression by reducing expression of the L-selectin lymph node (LN) homing receptor on naive T and B cells. MDSC-induced L-selectin loss occurs through a contact-dependent, post-transcriptional mechanism that is independent of the major L-selectin sheddase, ADAM17, but results in significant elevation of circulating L-selectin in tumor-bearing mice. Even moderate deficits in L-selectin expression disrupt T cell trafficking to distant LN. Furthermore, T cells preconditioned by MDSC have diminished responses to subsequent antigen exposure, which in conjunction with reduced trafficking, severely restricts antigen-driven expansion in widely-dispersed LN. These results establish novel mechanisms for MDSC-mediated immunosuppression that have unanticipated implications for systemic cancer immunity.
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