Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 117, Issue 11, Pages 3507-3518Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI32792
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Funding
- NCRR NIH HHS [P20 RR021905] Funding Source: Medline
- NIAID NIH HHS [R01 AI041747, AI045666, R01 AI051454, R56 AI051454, R01 AI058052, AI041747, AI058052, P01 AI045666, R21 AI051454, AI051454] Funding Source: Medline
- NINDS NIH HHS [R01 NS036526, NS036526] Funding Source: Medline
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Histamine receptor H-1 (H1R) is a susceptibility gene in both experimental autoimmune encephalomyelitis (EAE) and experimental autoimmune orchitis (EAO), 2 classical T cell-mediated models of organ-specific autoimmune disease. Here we showed that expression of H1R in naive CD4(+) T cells was required for maximal IFN-gamma production but was dispensable for proliferation. Moreover, H1R signaling at the time of TCR ligation was required for activation of p38 MAPK, a known regulator of IFN-gamma expression. Importantly, selective reexpression of H1R in CD4(+) T cells fully complemented both the IFN-gamma production and the EAE susceptibility of H1R-deficient mice. These data suggest that the presence of H1R in CD4(+) T cells and its interaction with histamine regulates early TCR signals that lead to Th1 differentiation and autoimmune disease.
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