Cutting Edge: CD4+CD25+ Regulatory T Cells Contribute to Gender Differences in Susceptibility to Experimental Autoimmune Encephalomyelitis

Authors

Jay Reddy, University of Nebraska-LincolnFollow
Hanspeter Waldner, Brigham and Women’s Hospital, Boston, MA
Xingmin Zhang, Brigham and Women’s Hospital, Boston, MA
Zsolt Illes, Brigham and Women’s Hospital, Boston, MA
Kai W. Wucherpfennig, Harvard Medical School, Boston, MAFollow
Raymond A. Sobel, Stanford University School of MedicineFollow
Vijay K. Kuchroo, Brigham and Women’s Hospital, Boston, MAFollow

Document Type

Article

Date of this Version

2005

Citation

Published in The Journal of Immunology 175:9 (2005), pp. 5591-5595; doi: 10.4049/ jimmunol.175.9.5591

Comments

Copyright © 2005 by The American Association of Immunologists, Inc. Used by permission.

Abstract

Female B10.S mice are highly resistant to proteolipid protein (PLP) 139–151-induced experimental autoimmune encephalomyelitis (EAE) and depletion of PLP 139–151- reactive CD4+CD25+regulatory T (Treg) cells can slightly increase their EAE susceptibility. Although male B10.S mice are moderately susceptible to EAE, we report that depletion of Treg cells in male B10.S mice before immunization with PLP 139–151 renders them highly susceptible to severe EAE with more CNS neutrophil infiltrates than nondepleted controls. Increased susceptibility is associated with an enhanced PLP 139–151-specific T cell response and greater production of IFN-γ, IL-6, and IL-17. Male CD4+CD25+ effector cells depleted of Treg cells proliferate to a greater degree than those from females in response to either anti-CD3 or PLP 139–151. These data suggest that because of their capacity to regulate potent autoaggressive effector cells, Treg cells partly contribute to the resistance to autoimmunity in the male mice.