| First Author | Chen Q | Year | 2000 |
| Journal | Nature | Volume | 407 |
| Issue | 6806 | Pages | 916-20 |
| PubMed ID | 11057672 | Mgi Jnum | J:65439 |
| Mgi Id | MGI:1926579 | Doi | 10.1038/35038103 |
| Citation | Chen Q, et al. (2000) Development of Th1-type immune responses requires the type I cytokine receptor TCCR. Nature 407(6806):916-20 |
| abstractText | On antigen challenge, T-helper cells differentiate into two functionally distinct subsets, Th1 and Th2, characterized by the different effector cytokines that they secrete. Th1 cells produce interleukin (IL)-2, interferon-gamma (IFN-gamma) and lymphotoxin-beta, which mediate pro-inflammatory functions critical for the development of cell-mediated immune responses, whereas Th2 cells secrete cytokines such as IL-4, IL-5 and IL-10 that enhance humoral immunity. This process of T-helper cell differentiation is tightly regulated by cytokines. Here we report a new member of the type I cytokine receptor family, designated T-cell cytokine receptor (TCCR). When challenged in vivo with protein antigen, TCCR-deficient mice had impaired Th1 response as measured by IFN-gamma production. TCCR-deficient mice also had increased susceptibility to infection with an intracellular pathogen, Listeria monocytogenes. In addition, levels of antigen-specific immunoglobulin-gamma2a, which are dependent on Th1 cells, were markedly reduced in these mice. Our results demonstrate the existence of a new cytokine receptor involved in regulating the adaptive immune response and critical to the generation of a Th1 response. |
