HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Barrington, R. A. Articles by Carroll, M. C. Search for Related Content PubMed PubMed Citation Articles by Barrington, R. A. Articles by Carroll, M. C.

Involvement of NFAT1 in B Cell Self-Tolerance¹

Robert A. Barrington^*, Madhuri Borde^*, Anjana Rao^* and Michael C. Carroll^2,*,

^* CBR Institute for Biomedical Research, Harvard University, Boston, MA 02115; and Department of Pathology, Harvard University, Boston, MA 02115 and Department of Pediatrics, Children’s Hospital, Boston, MA 02115

B cells from anti-lysozyme Ig/soluble lysozyme double-transgenic mice are chronically exposed to self-Ag in the periphery, resulting in an anergic phenotype. Chronic exposure to self-Ag leads to nuclear translocation of NFAT1 and NFAT2, suggesting that they are involved in anergy. To directly test a role for NFAT1 in B cell anergy, NFAT1-deficient mice were crossed with anti-lysozyme Ig transgenic mice. As expected, B cell anergy was evident in the presence of self-Ag based on reduced serum anti-lysozyme levels, percentage and number of mature B cells, and reduced B cell responsiveness. By contrast, B cell anergy was relieved in NFAT1^–/– mice expressing soluble self-Ag. Bone marrow development was equivalent in NFAT1-sufficient and -deficient mice, suggesting that loss of anergy in the latter is due to selection later in development. Taken together, these studies provide direct evidence that the transcription factor NFAT1 is involved in B cell anergy.