While transgenic mice expressing tumour necrosis factor-alpha under the control of the betacell-specific insulin promoter display a marked lymphocytic infiltration of the islets, they never develop insulin-dependent diabetes mellitus (IDDM). In striking contrast, "double" transgenic mice whose beta
In vivo depletion of CD4 and CD8 T lymphocytes impairsMycobacterium wvaccine-induced protection againstM. tubercolosisin mice
β Scribed by Indira Guleria; Rama Mukherjee; Stefan H. E. Kaufmann
- Publisher
- Springer-Verlag
- Year
- 1993
- Tongue
- English
- Weight
- 441 KB
- Volume
- 182
- Category
- Article
- ISSN
- 0300-8584
No coin nor oath required. For personal study only.
β¦ Synopsis
In the present study we sought to determine the relative role of CD4 and CD8 T cells in Mycobacterium w-induced protective immunity against tuberculosis of mice by in vivo depletion with specific monoclonal antibodies (mAb). Mice were immunized first with M. w, 4 weeks later treated with anti-CD4, anti-CD8 or a combination of both mAb and subsequently infected with M. tuberculosis H37Rv i.v. Numbers of colony-forming units in animals depleted of CD4 T cells, CD8 T cells or both T cell populations were significantly higher than those in control mice receiving irrelevant mAb or no mAb. Cytokine production by T cell subsets was also determined by culturing the cells remaining after in vivo depletion in the presence or absence of mycobacterial antigens. CD8 (CD4 depleted) T cells produced lower levels of interferon-y than CD4 (CD8 depleted) T cells. These data suggest that both CD4 and CD8 T cells participate in resistance against tuberculosis induced by vaccination with M. w.
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