Journal
JOURNAL OF IMMUNOLOGY
Volume 175, Issue 9, Pages 5591-5595Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.175.9.5591
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Funding
- NIAID NIH HHS [R01 AI44880] Funding Source: Medline
- NINDS NIH HHS [R01 NS44914, R01 NS30843, NS 046414, P01 NS38037] Funding Source: Medline
- PHS HHS [P01 A145757] Funding Source: Medline
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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-gamma, 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.
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