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Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Immunol 2014 ; 192 (12): 5679-86 Nephropedia Template TP
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Deletion of CD24 impairs development of heat shock protein gp96 -driven autoimmune disease through expansion of myeloid derived suppressor cells #MMPMID24808359
Thaxton JE; Liu B; Zheng P; Liu Y; Li Z
J Immunol 2014[Jun]; 192 (12): 5679-86 PMID24808359show ga
CD24 binds to and suppresses inflammation triggered by danger associated molecular patterns (DAMPS) such as heat-shock proteins (HSPs) and HMGB1. Paradoxically, CD24 has been shown to enhance autoimmune disease. Here we attempt to reconcile this paradox by deletion of CD24 (24KO) in a lupus-like disease model driven by forced expression of HSP gp96 at the cell surface (tm). As expected, tm24KO mice showed increased CD11c+ DC activation coupled to a significant increase in DC-specific IL-12 production compared to tm mice. However, tm24KO mice showed less CD4 T cell activation and peripheral inflammatory cytokine production in comparison to tm mice. We characterized an enhanced immune suppressive milieu in tm24KO mice distinguished by increased TGF-? and greater Treg suppressive capacity. We found greater absolute numbers of MDSCs in tm24KO mice and showed that the Ly6C+ MDSC subset had greater suppressive capacity from tm24KO mice. Deletion of CD24 in tm mice led to diminished lupus-like pathology as evidenced by anti-nuclear antibody deposition and glomerulonephritis. Finally, we show that expanded MDSC populations were mediated by increased free HMGB1 in tm24KO mice. Thus, the deletion of CD24 in an HSP-driven model of autoimmunity led to the unexpected development of Treg and MDSC populations that augmented immune tolerance. Further study of these populations as possible negative regulators of inflammation in the context of autoimmunity is warranted.