| pubmed-article:3097138 | pubmed:abstractText | In contrast to many other strains, inbred P strain mice fail to develop significant levels of resistance to challenge Schistosoma mansoni infection as a result of prior vaccination with radiation-attenuated cercariae. In this study, the relationship between defects in resistance and development of cell-mediated immune reactivity was examined. Although splenocytes from immunized P mice demonstrated deficiencies in production of macrophage-activating lymphokine(s) in response to either antigenic or mitogenic stimulation, other aspects of T lymphocyte responsiveness including blastogenesis, production of interleukin 2, interleukin 3 and macrophage chemotactic factor, as well as helper cell function for secondary plaque-forming cell response to a T-dependent antigen and allospecific cytolytic T cell reactivity, appeared to be comparable with those of C57BL/6 mice, a strain that is protected by vaccination against S. mansoni. FACS comparison revealed no significant deficits in percentages of Thy-1+, Lyt-1+, or L3T4+ splenocytes in vaccinated P mice. The P-associated defect in production of macrophage-activating factor appeared to be at the level of the T cell rather than the antigen-presenting cell, because macrophages from P mice could reconstitute the lymphokine-producing capacity of T-enriched splenocytes from immunized, resistant (C57BL/6 X P) F1 or B10.P mice, whereas the converse was not true. These results indicate that vaccinated P mice have a selective defect in T cell function for production of macrophage-activating lymphokine, which is manifested as a failure to produce activated larvicidal macrophages at the site of specific antigen challenge in vivo and may be associated with the failure of this strain to become resistant to S. mansoni. | lld:pubmed |
