期刊
JOURNAL OF IMMUNOLOGY
卷 178, 期 11, 页码 6710-6714出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.178.11.6710
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- NHLBI NIH HHS [HL70729, R01 HL087033, HL077611, HL087033] Funding Source: Medline
- NIEHS NIH HHS [ES03819, T32 ES07141] Funding Source: Medline
Recent clinical studies have reinforced the importance of sex-related differences in the pathogenesis of cardiovascular diseases, with an increased incidence and mortality in men. Similar to humans, male BALB/c mice infected with coxsackievirus B3 (CVB3) develop more severe inflammation in the heart even though viral replication is no greater than in females. We show that TLR4 and IFN-gamma levels are significantly elevated and regulatory T cell (Treg) populations significantly reduced in the heart of males following CVB3 infection, whereas females have significantly increased T cell Ig mucin (Tim)-3, IL-4 and Treg. Blocking Tim-3 in males significantly increases inflammation and TLR4 expression while reducing Treg. In contrast, defective TLR4 signaling significantly reduces inflammation while increasing Tim-3 expression. Cross-regulation of TLR4 and Tim-3 occurs during the innate and adaptive immune response. This novel mechanism may help explain why inflammatory heart disease is more severe in males.
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