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Multifocal defects in immune responses in RelB-deficient mice
1Department of Oncology, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, NJ 08543, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|June 1, 1997
Summary
Mice lacking the RelB protein showed increased susceptibility to bacterial and viral infections. This deficiency impaired crucial immune responses, including TNF-alpha production and T cell activity, highlighting RelB's role in immunity.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- The Rel/nuclear factor-kappaB (NF-κB) family, specifically RelB, plays a role in inflammatory responses.
- RelB-deficient mice exhibit myeloid hyperplasia and splenomegaly.
Purpose of the Study:
- To investigate the role of RelB in immune responses against bacterial and viral infections.
- To elucidate the impact of RelB deficiency on immune cell function and antibody production.
Main Methods:
- Generation and analysis of RelB-deficient mice.
- Infection models using Listeria monocytogenes and lymphocytic choriomeningitis virus.
- In vitro studies on macrophage TNF-alpha production.
- Analysis of antibody production.
Main Results:
- RelB-deficient mice displayed high susceptibility to Listeria monocytogenes infection.
- Impaired production of Tumor Necrosis Factor-alpha (TNF-α) by macrophages from RelB-deficient mice.
- Defective T cell-macrophage interactions and cytotoxic T cell responses observed.
- Normal production of IgG antibodies was dependent on RelB.
Conclusions:
- RelB is essential for normal hemopoiesis and innate immune responses.
- RelB plays a critical role in adaptive immunity, including T cell responses and antibody production.
- The absence of RelB significantly compromises the host's ability to combat infections.