| First Author | Frisancho-Kiss S | Year | 2007 |
| Journal | J Immunol | Volume | 178 |
| Issue | 11 | Pages | 6710-4 |
| PubMed ID | 17513715 | Mgi Jnum | J:147853 |
| Mgi Id | MGI:3842288 | Doi | 10.4049/jimmunol.178.11.6710 |
| Citation | Frisancho-Kiss S, et al. (2007) Cutting edge: cross-regulation by TLR4 and T cell Ig mucin-3 determines sex differences in inflammatory heart disease. J Immunol 178(11):6710-4 |
| abstractText | 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. |
