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Differential antigen recognition by T cell populations from strains of mice developing polar forms of granulomatous inflammation in response to eggs of Schistosoma mansoni
Author(s) -
Hernandez Hector J.,
Trzyna Wendy C.,
Cordingley John S.,
Brodeur Peter H.,
Stadecker Miguel J.
Publication year - 1997
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830270314
Subject(s) - biology , schistosoma mansoni , antigen , congenic , immunology , t cell , major histocompatibility complex , monoclonal antibody , polyclonal antibodies , schistosomiasis , virology , antibody , immune system , gene , helminths , genetics
Abstract 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‐A k or I‐E k , 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‐2 k 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.