| First Author | Hernandez HJ | Year | 1997 |
| Journal | Eur J Immunol | Volume | 27 |
| Issue | 3 | Pages | 666-70 |
| PubMed ID | 9079807 | Mgi Jnum | J:39003 |
| Mgi Id | MGI:86389 | Doi | 10.1002/eji.1830270314 |
| Citation | Hernandez HJ, et al. (1997) Differential antigen recognition by T cell populations from strains of mice developing polar forms of granulomatous inflammation in response to eggs of Schistosoma mansoni. Eur J Immunol 27(3):666-70 |
| abstractText | In humans, infection with schistosome helminths can lead to dissimilar forms of clinical disease. Likewise, in the experimental mouse system, identical infection protocols with Schistosoma mansoni cause a more severe granulomatous disease in the C3H strain than in the C57BL/6 strain. To address this difference, we developed panels of schistosomal egg antigen (SEA)-specific T cell hybridomas to compare the responses of C3H and C57BL/6 mice to the major egg antigen p40. All derived C3H T cell hybridomas, despite being clonally distinct and restricted by either I-Ak or I-Ek, responded to recombinant fragment 15-1 of the p40 antigen, while none of the C57BL/6 T cell hybridomas did. Consistent with the observed monoclonal T cell responses, polyclonal lymph node cells from schistosome-infected C3H mice reacted strongly to fragment 15-1, which contrasted sharply with the weak response displayed by the C57BL/6 strain. Moreover, studies with congenic mice demonstrated that the strong CD4+ T cell response to fragment 15-1 was under major histocompatibility complex control and segregated with the H-2k haplotype. These findings suggest that a dominant T cell response against a major egg antigen may represent a risk factor for the development of severe disease. |
