Requirement for the NF-kappa B family member Re1A in the development of secondary lymphoid organs
Abstract
The transcription factor nuclear factor (NF)-kappaB has been suggested to be a key mediator of the development of lymph nodes and Peyer's patches. However, targeted deletion of NF-kappaB/ Rel family members has not yet corroborated such a function. Here we report that when mice lacking the RelA subunit of NF-kappaB are brought to term by breeding onto a tumor necrosis factor receptor (TNFR)1-deficient background, the trice that are born lack lymph nodes, foyer's patches, and an organized splenic microarchitecture, and have a profound defect in T cell-dependent antigen responses. Analyses of TNFR1/1RelA-deficient embryonic tissues and of radiation chimeras suggest that the dependence on RelA is manifest not in hematopoietic cells but rather in radioresistant stromal cells needed for the development of secondary lymphoid organs.
Additional Information
© 2002 Rockefeller University Press. Submitted: November 13, 2001; accepted: November 30, 2001. We wish to thank Jeffrey L. Browning and colleagues at Biogen, Inc. for creating, characterizing, and producing LT-specific reagents; Denise Crowley for advice on immunohistochemistry; Jianzhu Chen for advice on antibody analysis; Paul Majewski for technical assistance; and Stephen Robinson for helpful suggestions and critical review of this work as it progressed. This work was supported by the National Institutes of Health grants (to D. Baltimore and E. Alcamo), and by grants from the Whitehead Institute Fellows Program, Hascoe Foundation, and Rippel Foundation (to N. Hacohen).Attached Files
Published - ALCjem02.pdf
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Additional details
- PMCID
- PMC2193608
- Eprint ID
- 5111
- Resolver ID
- CaltechAUTHORS:ALCjem02
- NIH
- Whitehead Institute for Biomedical Research
- Hascoe Foundation
- Rippel Foundation
- Created
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2006-10-02Created from EPrint's datestamp field
- Updated
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2021-11-08Created from EPrint's last_modified field