| First Author | Blum AM | Year | 2003 |
| Journal | Am J Physiol Gastrointest Liver Physiol | Volume | 284 |
| Issue | 2 | Pages | G197-204 |
| PubMed ID | 12388184 | Mgi Jnum | J:107858 |
| Mgi Id | MGI:3622387 | Doi | 10.1152/ajpgi.00271.2002 |
| Citation | Blum AM, et al. (2003) T cell substance P receptor governs antigen-elicited IFN-gamma production. Am J Physiol Gastrointest Liver Physiol 284(2):G197-204 |
| abstractText | Substance P (SP) enhances antigen-dependent T cell IFN-gamma production. It was determined if a T cell neurokinin-1 receptor (NK-1R) was critical for IFN-gamma regulation. T cells from schistosome-infected mice were mixed with splenocytes from uninfected NK-1R knockout (KO) animals. Thus only the schistosome egg antigen-specific T cells expressed NK-1R. The cells were cultured 18 h with or without SP. SP enhanced antigen-induced IFN-gamma production fourfold without affecting IL-4 or IL-5 secretion. NK-1R inhibitor blocked this stimulation. Neither purified T cells nor naive KO splenocytes cultured alone responded to antigen. To further define the importance of T cell NK-1R, we developed a T cell-selective NK-1R KO mouse by reconstituting T cell-deficient Rag mice with NK-1R KO T cells. These mice challanged with schistosomiasis developed abnormal liver granulomas. Granuloma size was smaller in T cell-selective NK-1R KO mice compared with granulomas in Rag reconstituted with normal T cells. Splenocytes and granuloma cells from NK-1R KO mice made less IFN-gamma. The mice also made less IgG2a. Thus T cell NK-1R is important for IFN-gamma regulation. |
