IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kamath, A. B.
Right arrow Articles by Behar, S. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kamath, A. B.
Right arrow Articles by Behar, S. M.

 Previous Article  |  Next Article 

Infection and Immunity, September 2005, p. 6110-6118, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.6110-6118.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Anamnestic Responses of Mice following Mycobacterium tuberculosis Infection

Arati B. Kamath and Samuel M. Behar*

Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115

Received 21 December 2004/ Returned for modification 8 February 2005/ Accepted 16 May 2005

The anamnestic response is the property of the immune system that makes vaccine development possible. Although the development of a vaccine against Mycobacterium tuberculosis is an important global priority, there are many gaps in our understanding of how immunological memory develops following M. tuberculosis infection or after BCG vaccination. In experiments designed to compare the anamnestic response of susceptible and resistant mouse strains, major histocompatibility complex-matched memory-immune C3.SW-H2b/SnJ and C57BL/6 mice both demonstrated better control of bacterial replication following reinfection with M. tuberculosis than control mice. Nevertheless, this memory response did not appear to have any long-term protective effect for either mouse strain. A greater understanding of the immunological factors that govern the maintenance of immunological memory following exposure to M. tuberculosis will be required to develop an effective vaccine.

* Corresponding author. Mailing address: Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Smith Building Room 516C, One Jimmy Fund Way, Boston, MA 02115. Phone: (617) 525-1033. Fax: (617) 525-1010. E-mail: sbehar{at}rics.bwh.harvard.edu.

Editor: J. L. Flynn

Infection and Immunity, September 2005, p. 6110-6118, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.6110-6118.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2005 by the American Society for Microbiology. All rights reserved.