This Article Full Text (PDF) Other Versions of this Article: IAI.01709-06v1 75/5/2260    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Anis, M. M. Articles by Boom, W. H. Search for Related Content PubMed PubMed Citation Articles by Anis, M. M. Articles by Boom, W. H.

 Previous Article  |  Next Article 

Infect. Immun. doi:10.1128/IAI.01709-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Modulation of naïve CD4+ T cell responses to an airway antigen during pulmonary mycobacterial infection

Department of Pathology, Division of Infectious Diseases, and Tuberculosis Research Unit, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, Ohio

^* To whom correspondence should be addressed. Email: whb{at}cwru.edu.

	Abstract

During pulmonary mycobacterial infection, there is increased trafficking of dendritic cells from the lungs to the draining lymph nodes. We hypothesized that ongoing mycobacterial infection would modulate recruitment and activation of antigen-specific naïve CD4+ T cells after airway antigen challenge. BALB/c mice were infected by aerosol with Mycobacterium bovis-BCG. At peak bacterial burden in the lungs (4-6 wks. post-infection), CFSE-labeled naïve ovalbumin-specific DO11.10 T cells were adoptively transferred into infected and uninfected mice. Recipient mice were challenged intranasally with soluble ovalbumin (OVA) and OVA-specific T cell responses were measured in lung, draining mediastinal lymph node (MLN) and spleen. OVA challenge resulted in increased activation and proliferation of OVA-specific T cells in the draining MLNs of both infected and uninfected mice. However, only BCG-infected mice had prominent OVA-specific T cell activation, proliferation, and T_h1 differentiation in the lungs. BCG infection caused greater distribution of airway-OVA to pulmonary dendritic cells and enhanced presentation of OVA peptide by lung CD11c+ cells. Together these data suggest that an existing pulmonary mycobacterial infection alters the phenotype of lung dendritic cells so that they can activate antigen-specific naïve CD4+ T cells in the lungs in response to airway antigen challenge.

This article has been cited by other articles:

• Anis, M. M., Fulton, S. A., Reba, S. M., Liu, Y., Harding, C. V., Boom, W. H. (2008). Modulation of Pulmonary Dendritic Cell Function during Mycobacterial Infection. Infect. Immun. 76: 671-677 [Abstract] [Full Text]