TY - JOUR
T1 - Overproduction of corticotropin-releasing hormone blocks germinal center formation
T2 - Role of corticosterone and impaired follicular dendritic cell networks
AU - Murray, Susan E.
AU - Rosenzweig, Holly L.
AU - Johnson, Martha
AU - Huising, Mark O.
AU - Sawicki, Kristine
AU - Stenzel-Poore, Mary P.
N1 - Funding Information:
This project was supported by grants from NIMH: RO1 MH55722 (M.S.-P.) and NIAIDE: T32 A107472 (S.E.M.). We greatly appreciate the immunofluorescent analysis of splenic architecture provided by John Kearney. We thank Marvin B. Rittenberg for insightful discussions, critical review of the manuscript and T15 monoclonal antibodies. We also thank Greg Wiens and McKay Brown for technical advice, Sarah Coste for editorial expertise, and Marie Kosco-Vilbois for FDC-M1 monoclonal antibody used in pilot experiments.
PY - 2004/11
Y1 - 2004/11
N2 - Corticotropin-releasing hormone (CRH) is a central mediator in the response to stress, coordinating behavioral, autonomic and neuroendocrine activation. CRH overproduction is implicated in several affective disorders, including major depression, panic-anxiety disorder and anorexia-diseases also associated with altered immune function. We investigated the link between CRH overdrive and immune function using CRH transgenic mice. Following immunization, CRH transgenic mice fail to form germinal centers; chronic glucocorticoid administration recapitulates this effect in wild-type mice. Regulation of germinal centers by glucocorticoids appears to be mediated, in part, through effects on follicular dendritic cells (FDC), providing a novel mechanism by which CRH dysregulation may significantly impair humoral immune responses.
AB - Corticotropin-releasing hormone (CRH) is a central mediator in the response to stress, coordinating behavioral, autonomic and neuroendocrine activation. CRH overproduction is implicated in several affective disorders, including major depression, panic-anxiety disorder and anorexia-diseases also associated with altered immune function. We investigated the link between CRH overdrive and immune function using CRH transgenic mice. Following immunization, CRH transgenic mice fail to form germinal centers; chronic glucocorticoid administration recapitulates this effect in wild-type mice. Regulation of germinal centers by glucocorticoids appears to be mediated, in part, through effects on follicular dendritic cells (FDC), providing a novel mechanism by which CRH dysregulation may significantly impair humoral immune responses.
KW - Antibodies
KW - B lymphocytes
KW - Follicular dendritic cell
KW - Germinal center
KW - Immunization
KW - Transgenic
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U2 - 10.1016/j.jneuroim.2004.06.015
DO - 10.1016/j.jneuroim.2004.06.015
M3 - Article
C2 - 15465594
AN - SCOPUS:4744339249
SN - 0165-5728
VL - 156
SP - 31
EP - 41
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 1-2
ER -