T cell subset-dependent modulation of immunity to Borrelia burgdorferi in mice.

A Keane-Myers, SP Nickell - Journal of immunology (Baltimore, Md …, 1995 - journals.aai.org
A Keane-Myers, SP Nickell
Journal of immunology (Baltimore, Md.: 1950), 1995journals.aai.org
The possible involvement of specific T cells in resolution of infections with Borrelia
burgdorferi (Bb), the causative agent of human Lyme disease, has not been adequately
studied. To investigate the potential role of T cell subsets in resistance, we have depleted
mice of CD4+ and CD8+ T cell subsets in vivo by the administration of specific mAbs and
have examined outcomes after infection with Bb. Our results indicate that CD4+ T cells are
required for immunologic control of spirochete levels, because their depletion in both …
Abstract
The possible involvement of specific T cells in resolution of infections with Borrelia burgdorferi (Bb), the causative agent of human Lyme disease, has not been adequately studied. To investigate the potential role of T cell subsets in resistance, we have depleted mice of CD4+ and CD8+ T cell subsets in vivo by the administration of specific mAbs and have examined outcomes after infection with Bb. Our results indicate that CD4+ T cells are required for immunologic control of spirochete levels, because their depletion in both susceptible C3H/HeN and resistant BALB/c mice increased the severity of arthritis and the numbers of spirochetes found in joints and skin, as compared with Bb-infected mice treated with a control mAb. In contrast, the CD8+ T cell compartment, particularly in susceptible C3H/HeN mice, appears to promote the disease process, possibly by interfering with the generation of protective immunity, as abrogation of this subset in vivo led to a reduction in both arthritis and in spirochete levels found in joints and skin when compared with Bb-infected control mice. Our inability to establish a correlation between resistance and Bb-specific IgG Ab levels in these mice raises the possibility that Ab-independent mechanisms are important in protection. These findings suggest that the final outcome in Bb-infected hosts may be the net effect of antagonistic influences exerted by CD4+ and CD8+ T cell subsets.
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