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CD4 expression is important but not essential for infection with exogenous mouse mammary tumor virus
Y Ando1, W Wajjwalku, K Kishihara
1Department of Pediatrics, Nagoya University School of Medicine, Japan.
Abstract:
We studied local events in the popliteal lymph nodes of CD4-deficient mice following foot pad injection with an MMTV strain which carries the gene for a V beta 14-specific superantigen. Injection of the V beta 14-specific MMTV induced vigorous expansion of V beta 14+ CD4+ T cells and B cells in their lymph nodes of CD4+/- heterozygous control mice. On the other hand, CD4-/- mice injected with the MMTV showed a proliferation of V beta 14+ T cells among the population of TCR alpha beta + CD4-CD8- T cells, although to a lesser extent. This phenomenon was not accompanied by vigorous B cell expansion. A PCR assay revelated that the MMTV definitely infected the lymph nodes cells of the CD4-/- mouse. However, the infectivity of the MMTV in CD4-/- mice was approximately 20 times lower than that in CD4+/- mice. These findings indicate that, in MMTV infection of CD4-deficient mice, the superantigen-reactive T cells among the population of TCR alpha beta +CD4-CD8- T cells substitute for the superantigen-reactive CD4- T cells of normal mice, and that the absence of CD4 molecules decreased the infectivity of MMTV because of insufficient expansion of the superantigen-reactive T cells.
Insights
CD4-deficient mice infected with mammary tumor virus (MMTV) showed T cell proliferation in lymph nodes. Superantigen-reactive T cells compensated for the lack of CD4+ T cells, but MMTV infectivity was reduced.
Area of Science:
- Immunology
- Virology
- Mouse Models
Background:
- Murine mammary tumor virus (MMTV) utilizes superantigens to stimulate T cells.
- CD4+ T cells are critical for adaptive immune responses and MMTV infection.
Purpose of the Study:
- To investigate the role of CD4+ T cells in MMTV infection in CD4-deficient mice.
- To analyze T cell and B cell responses in the popliteal lymph nodes following MMTV infection.
Main Methods:
- Footpad injection of MMTV into CD4-deficient (CD4-/-) and heterozygous (CD4+/-) mice.
- Analysis of T cell (V beta 14+, TCR alpha beta +CD4-CD8-) and B cell populations in lymph nodes.
- Polymerase Chain Reaction (PCR) to assess MMTV infectivity.
Main Results:
- CD4+/- mice showed robust expansion of V beta 14+ CD4+ T cells and B cells.
- CD4-/- mice exhibited proliferation of V beta 14+ T cells within the TCR alpha beta +CD4-CD8- population, but with less B cell expansion.
- MMTV infectivity was approximately 20-fold lower in CD4-/- mice compared to CD4+/- mice.
Conclusions:
- In CD4-deficient mice, TCR alpha beta +CD4-CD8- T cells can substitute for CD4+ T cells in response to MMTV superantigens.
- The absence of CD4 molecules impairs MMTV infectivity due to insufficient expansion of superantigen-reactive T cells.