Human alveolar T lymphocyte responses to Mycobacterium tuberculosis antigens: role for CD4+ and CD8+ cytotoxic T cells and relative resistance of alveolar macrophages to lysis.

Tan, JS and Canaday, DH and Boom, WH and Balaji, KN and Schwander, SK and Rich, EA. (1997) Human alveolar T lymphocyte responses to Mycobacterium tuberculosis antigens: role for CD4+ and CD8+ cytotoxic T cells and relative resistance of alveolar macrophages to lysis. In: The Journal of Immunology, 159 (1). pp. 290-297.

PDF 290.pdf - Published Version Restricted to Registered users only Download (915kB) | Request a copy

Abstract

T cell-mediated cytotoxicity against Mycobacterium tuberculosis (MTB)-infected macrophages may be a major mechanism of specific host defense, but little is known about such activities in the lung. Thus, the capacity of alveolar lymphocyte MTB-specific cell lines (AL) and alveolar macrophages (AM) from tuberculin skin test-positive healthy subjects to serve as CTL and target cells, respectively, in response to MTB (H37Ra) or purified protein derivative (PPD) was investigated. Mycobacterial Ag-pulsed AM were targets of blood CTL activity at E:T ratios of > or = 30:1 (51Cr release assay), but were significantly more resistant to cytotoxicity than autologous blood monocytes. PPD- plus IL-2-expanded AL and blood lymphocytes were cytotoxic for autologous mycobacterium-stimulated monocytes at E:T ratios of > or = 10:1. The CTL activity of lymphocytes expanded with PPD was predominantly class II MHC restricted, whereas the CTL activity of lymphocytes expanded with PPD plus IL-2 was both class I and class II MHC restricted. Both CD4+ and CD8+ T cells were enriched in BL and AL expanded with PPD and IL-2, and both subsets had mycobacterium-specific CTL activity. Such novel cytotoxic responses by CD4+ and CD8+ T cells may be a major mechanism of defense against MTB at the site of disease activity.

Item Type:	Journal Article
Publication:	The Journal of Immunology
Publisher:	American Association of Immunologists
Additional Information:	Copyright of this article belongs to American Association of Immunologists.
Department/Centre:	Division of Biological Sciences > Microbiology & Cell Biology
Date Deposited:	19 Feb 2010 11:05
Last Modified:	19 Sep 2010 05:55
URI:	http://eprints.iisc.ac.in/id/eprint/25687

Actions (login required)

View Item