RT Journal Article SR Electronic T1 C-Reactive Protein Directly Suppresses Th1 Cell Differentiation and Alleviates Experimental Autoimmune Encephalomyelitis JF The Journal of Immunology JO J. Immunol. FD American Association of Immunologists SP 5243 OP 5252 DO 10.4049/jimmunol.1402909 VO 194 IS 11 A1 Zhang, Lin A1 Liu, Shan-Hui A1 Wright, Tyler T. A1 Shen, Zhi-Yuan A1 Li, Hai-Yun A1 Zhu, Wei A1 Potempa, Lawrence A. A1 Ji, Shang-Rong A1 Szalai, Alexander J. A1 Wu, Yi YR 2015 UL http://www.jimmunol.org/content/194/11/5243.abstract AB Human C-reactive protein (CRP) is a serum-soluble pattern recognition receptor that serves as a marker of inflammation and directly contributes to innate immunity. In this study, we show that human CRP also directly contributes to adaptive immunity, that is, native CRP binds specifically to human Jurkat T cells and to mouse naive CD4+ T cells and modulates their Th1 and Th2 responses. In vitro both exogenously added (purified) and endogenously expressed (via transfection) human CRP inhibited Th1 differentiation and augmented Th2 differentiation of naive CD4+ T cells. In vivo for human CRP transgenic compared with wild-type mice, a lesser proportion of the T cells recovered from the spleens of healthy animals were Th1 cells. Moreover, in both CRP transgenic mice and in wild-type mice treated with human CRP, during myelin oligodendrocyte glycoprotein peptide–induced experimental autoimmune encephalomyelitis both the Th1 cell response and disease severity were inhibited. These pattern recognition–independent actions of CRP directly on T cells highlights the potential for this soluble pattern recognition receptor to act as a tonic regulator of immunity, shaping global adaptive immune responses during both homeostasis and disease.