Abstract
One of the major models used to study mechanisms of immunity to viruses is infection of mice by lymphocytic choriomeningitis virus (LCMV). Studies in mice have been used to show the critical role of CD8 T cells and the effector mechanisms that are used in viral clearance. However, the immune response to viruses is being dissected further, and a recent paper by Homann et al.1xEvidence of an underlying CD4 helper and CD8 T-cell defect in B-cell-deficient mice: failure to clear persistent virus infection after adoptive immunotherapy with virus-specific memory cells from μMT/μMT mice. Homann, D. et al. J. Virol. 1998; 72: 9208–9216PubMedSee all References1 typifies this. The authors have taken memory immune T cells from B-cell deficient (μMT) mice and shown that these cells are unable to aid the clearance of LCMV after transfer into persistently infected mice. However, B cells are not necessary for virus clearance when wild-type lymphocytes are transferred. The inability of μMT memory T cells to clear LCMV from recipient mice is linked to decreased CD4 T-helper cell functions and reduced cytokine production by CD8 T cells. The authors suggest that this shows a role for B cells in development and maintenance of T-cell function. However, there are other abnormalities within μMT mice. These mice lack follicular dendritic cells, which capture and hold antigen in lymphoid tissues. Some of the above defects might therefore result from reduced levels of antigen after viral clearance rather than a lack of B cells per se.
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