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Infection and Immunity, October 2009, p. 4469-4479, Vol. 77, No. 10
0019-9567/09/$08.00+0     doi:10.1128/IAI.00491-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Chlamydia muridarum-Specific CD4 T-Cell Clones Recognize Infected Reproductive Tract Epithelial Cells in an Interferon-Dependent Fashion{triangledown}

Krupakar Jayarapu,1 Micah S. Kerr,1 Adrian Katschke,2 and Raymond M. Johnson1*

Department of Medicine,1 Department of Biostatistics, Indiana University School of Medicine, Indianapolis, Indiana 462022

Received 4 May 2009/ Returned for modification 20 July 2009/ Accepted 3 August 2009

During natural infections Chlamydia trachomatis urogenital serovars replicate predominantly in the epithelial cells lining the reproductive tract. This tissue tropism poses a unique challenge to host cellar immunity and future vaccine development. In the experimental mouse model, CD4 T cells are necessary and sufficient to clear Chlamydia muridarum genital tract infections. This implies that resolution of genital tract infection depends on CD4 T-cell interactions with infected epithelial cells. However, no laboratory has shown that Chlamydia-specific CD4 T cells can recognize Chlamydia antigens presented by major histocompatibility complex class II (MHC-I) molecules on epithelial cells. In this report we show that MHC-II-restricted Chlamydia-specific CD4 T-cell clones recognize infected upper reproductive tract epithelial cells as early as 12 h postinfection. The timing of recognition and degree of T-cell activation are dependent on the interferon (IFN) milieu. Beta IFN (IFN-β) and IFN-{gamma} have different effects on T-cell activation, with IFN-β blunting IFN-{gamma}-induced upregulation of epithelial cell surface MHC-II and T-cell activation. Individual CD4 T-cell clones differed in their degrees of dependence on IFN-{gamma}-regulated MHC-II for controlling Chlamydia replication in epithelial cells in vitro. We discuss our data as they relate to published studies with IFN knockout mice, proposing a straightforward interpretation of the existing literature based on CD4 T-cell interactions with the infected reproductive tract epithelium.

* Corresponding author. Mailing address: Division of Infectious Diseases, Department of Medicine, Indiana University School of Medicine, 545 Barnhill Drive, #435, Indianapolis, IN 46202. Phone: (317) 278-6968. Fax: (317) 274-1587. E-mail: raymjohn{at}iupui.edu

{triangledown} Published ahead of print on 10 August 2009.

Editor: R. P. Morrison

Infection and Immunity, October 2009, p. 4469-4479, Vol. 77, No. 10
0019-9567/09/$08.00+0     doi:10.1128/IAI.00491-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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