| Abstrakt: |
C57BL/6 mice infected with a murine leukemia virus (MuLV) mixture designated LP-BM5 develop an immunodeficiency syndrome termed MAIDS, characterized by a variety of T and B cell abnormalities, including elevated levels of IgE, suggesting that IL-4 expression is increased in these animals. It has been suggested that the immunodeficiency associated with MAIDS is caused by a conversion of immune responses normally characterized by T1 development towards a T2- dominated response. Mice of the same strain, infected with , mount a protective T1 response with the induction of high levels of IFN-γ and undetectable IL-4. We therefore infected mice with at differing time points before and after virus infection and assessed the effects on T cell responsiveness, cytokine production and survival to , as well as the effect on MAIDS-associated pathology. We have also immunized C57BL/6 mice with trinitrophenol-keyhole limpet haemocyanln (TNP-KLH), which leads to a predominantly T2 response, and compared the effects of MAIDS on the response to TNP-KLH with the effect of MAIDS on infection. Our results show that significant immunodeficiency with regard to infection by is only apparent after 8 weeks of LP-BM5 MuLV infection, by which time T and B cell defects are well advanced. Further, we have found that the strongly polarized T1 response stimulated by infection can modulate the effect of MAIDS on T cells, leading to the survival of antigen-specific T cells. Our results suggest that the impairment of immune responses to either TNP–KLH or is due not to an alteration of the balance of T1/T2 subsets but to a general loss of reactivity in antigen-specific CD4 cells. However, prior activation of T1 but not T2 cells can inhibit the development of lymphoproliferation and immunodeficiency caused by MAIDS. [ABSTRACT FROM PUBLISHER] |
