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Published January 27, 1995 | public
Journal Article

Targeted disruption of the p50 subunit of NF-κB leads to multifocal defects in immune responses

Abstract

NF-κB, a heterodimeric transcription factor composed of p50 and p65 subunits, can be activated in many cell types and is thought to regulate a wide variety of genes involved in immune function and development. Mice lacking the p50 subunit of NF-κB show no developmental abnormalities, but exhibit multifocal defects in immune responses involving B lymphocytes and nonspecific responses to infection. B cells do not proliferate in response to bacterial lipopolysaccharide and are defective in basal and specific antibody production. Mice lacking p50 are unable effectively to clear L. monocytogenes and are more susceptible to infection with S. pneumoniae, but are more resistant to infection with murine encephalomyocarditis virus. These data support the role of NF-κB as a vital transcription factor for both specific and nonspecific immune responses, but do not indicate a developmental role for the factor.

Additional Information

© 1995 by Cell Press. Received 22 August 1994, Revised 8 November 1994. Correspondence should be addressed to D. B. We thank Andy Plump and the transgenic facility at The Rockefeller University for help in embryonic stem cell culture and generation of mutant mice; Karen Sokol for gross and histological analyses; Alan Aderem and Nurin Veis for help with macrophage studies; the laboratory of Ralph Steinman for help with flow cytometry and cellular assays; Robert Schreiber for help and advice with cytokine assays; Clifford Snapper for helpful discussion; Joshy Jacob for help with immunizations; Raul Andino for help with EMC virus; Martin Scott for help with pathogen challenge experiments; Eugenia Spanopolou and Chris Roman for RAG1^(-/-) mice; and members of the Baltimore lab for review of the manuscript. W. C. S. is supported by a fellowship from National Institutes of Health (NIH) grant AI08724-02; H.-C. L. is a fellow of the Cancer Research Institute; this work was supported by NIH grant GM39458 to D. B.

Additional details

Created:
August 20, 2023
Modified:
October 20, 2023