The Journal of Experimental Medicine
Avanti Polar Lipids, Inc.
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

Published online
doi:10.1084/jem.20080979
The Journal of Experimental Medicine, Vol. 205, No. 13, 3053-3064
The Rockefeller University Press, 0022-1007 $30.00
© Choi et al.
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 2227K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Choi, Y. S.
Right arrow Articles by Baumgarth, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Choi, Y. S.
Right arrow Articles by Baumgarth, N.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

ARTICLE

Dual role for B-1a cells in immunity to influenza virus infection

Youn Soo Choi1,2 and Nicole Baumgarth1,2,3

1 Graduate Group in Immunology, 2 Center for Comparative Medicine, and 3 Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, Davis, CA 95616

CORRESPONDENCE Nicole Baumgarth: nbaumgarth{at}ucdavis.edu

B-1 cells are known to contribute most of the "natural antibodies" that are secreted in the steady state, antibodies which are crucial for protection against many pathogens including influenza virus. Whether the CD5+ B-1a subset plays a role during an active immune response is incompletely understood. In contrast to recent data suggesting a passive role for B-1a cells, data provided here show strong highly localized activation of B-1 cells in the draining lymph nodes of the respiratory tract after influenza infection. B-1 cells are identified as a major source for both steady state and infection-induced local virus-neutralizing IgM. The CD5+ B-1a subset is the main B-1 cell subset generating this response. B-1a cell responses are generated by their increased local accumulation rather than by antigen-specific expansion. Our study reveals that during infection with influenza, CD5-expressing B-1a cells respond to and contribute to protection, presumably without the need for B cell receptor–mediated antigen-specific signals, which are known to induce the death of B-1a cells rather than activation. With that, our data reveal fundamental differences in the response regulation of B-1 and B-2 cells during an infection.


Abbreviations used: AFC, antibody-forming cell; BAL, bronchoalveolar lavage; BCR, B cell receptor; BLF, BAL fluid; GC, germinal center; HI, hemagglutination inhibition; MedLN, mediastinal LN; PerC, peritoneal cavity wash out cell; PLN, peripheral LN.

© 2008 Choi and Baumgarth This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS