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.