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c-Rel is essential for B lymphocyte survival and cell cycle progression
J R Tumang1, A Owyang, S Andjelic
1Graduate School of Medical Sciences, Weill Medical College of Cornell University, New York, NY 10021, USA.
European Journal of Immunology
|December 23, 1998
Summary
The transcription factor c-Rel is essential for B cell function, impacting germinal center and memory cell formation. Mice lacking c-Rel show impaired B cell proliferation and survival signaling.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- c-Rel is a lymphoid-specific transcription factor within the NF-kappaB/Rel family.
- Understanding c-Rel's role is crucial for B lymphocyte function and immune responses.
Purpose of the Study:
- To investigate the function of c-Rel in B lymphocyte development and immune responses.
- To elucidate the molecular mechanisms underlying c-Rel's role in B cell signaling.
Main Methods:
- Gene targeting to create c-Rel knockout (c-Rel-/-) mice.
- Flow cytometry to analyze B cell populations (memory, germinal center).
- In vitro assays to assess B cell proliferation, survival, and signaling.
Main Results:
- c-Rel-/- mice exhibit reduced B cells with memory and germinal center phenotypes.
- c-Rel-/- B cells show poor proliferation and diminished early molecular responses to IgM, CD40, LPS, or T cell help.
- c-Rel-/- B cells have impaired survival signaling from anti-IgM and LPS but normal CD40-mediated survival.
- Co-stimulation rescues cell cycle progression in c-Rel-/- B cells, indicating intrinsic defects.
Conclusions:
- c-Rel is indispensable for germinal center and memory B cell differentiation in vivo.
- c-Rel is required for B cell survival and cell cycle progression signals mediated by anti-IgM and LPS in vitro.
- c-Rel plays a role in CD40-induced proliferation but not CD40-mediated survival signals.