This Article Full Text Full Text (PDF) All Versions of this Article: 2005-0198OCv1 34/2/167    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 Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wieland, C. W. Articles by van der Poll, T. Search for Related Content PubMed PubMed Citation Articles by Wieland, C. W. Articles by van der Poll, T.

CD4⁺ Cells Play a Limited Role in Murine Lung Infection with Mycobacterium kansasii

Laboratory of Experimental Internal Medicine, Department of Pathology, and Department of Internal Medicine, Division of Infectious Diseases, Tropical Medicine, and AIDS, Academic Medical Center, University of Amsterdam, The Netherlands

Correspondence and requests for reprints should be addressed to Catharina W. Wieland, Laboratory of Experimental Internal Medicine, G2-132, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. E-mail: c.wieland{at}amc.uva.nl

Mycobacterium kansasii has emerged as an important nontuberculous mycobacterium that can cause severe infection in the immunocompromised host, especially in human immunodeficiency virus–infected patients. However, little is known about the pathogenesis of this infection. Because patients suffering from M. kansasii infection are severely compromised in their cellular immune response, we studied the course of infection in CD4⁺ cell knockout (KO) mice. Wild-type (WT) mice and CD4⁺ KO mice were infected with 10⁵ cfu of M. kansasii. Although previously shown to be susceptible to Mycobacterium tuberculosis infection, CD4⁺ KO mice demonstrated no impairment in clearing infection with M. kansasii when compared with WT animals, despite reduced pulmonary inflammation (reduced granuloma formation and lymphocyte infiltration in the lungs). Pulmonary IFN- levels and M. kansasii–induced IFN- production by splenocytes from infected animals were reduced in CD4⁺ KO mice, confirming that these mice were defective in the M. kansasii–specific T helper cell type 1 immune response. Furthermore, mice deficient for IFN-, IL-12p35, IL-12p40, or IL-18 also displayed a normal host defense against pulmonary infection with M. kansasii. These data suggest that CD4⁺ cells, IFN-, and an intact T helper cell type 1 response play a limited role in protective immunity against pulmonary M. kansasii infection.

Key Words: CD4 • IFN- • infection • mycobacterium • T helper cell type 1 response

This article has been cited by other articles:

				R. M. Wosten-van Asperen, R. Lutter, J. J. Haitsma, M. P. Merkus, J. B. van Woensel, C. M. van der Loos, S. Florquin, B. Lachmann, and A. P. Bos ACE mediates ventilator-induced lung injury in rats via angiotensin II but not bradykinin Eur. Respir. J., February 1, 2008; 31(2): 363 - 371. [Abstract] [Full Text] [PDF]