Publication Date:
1997-06-13
Description:
In analyzing mechanisms of protection against intracellular infections, a series of human CD1-restricted T cell lines of two distinct phenotypes were derived. Both CD4(-)CD8(-) (double-negative) T cells and CD8(+) T cells efficiently lysed macrophages infected with Mycobacterium tuberculosis. The cytotoxicity of CD4(-)CD8(-) T cells was mediated by Fas-FasL interaction and had no effect on the viability of the mycobacteria. The CD8(+) T cells lysed infected macrophages by a Fas-independent, granule-dependent mechanism that resulted in killing of bacteria. These data indicate that two phenotypically distinct subsets of human cytolytic T lymphocytes use different mechanisms to kill infected cells and contribute in different ways to host defense against intracellular infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stenger, S -- Mazzaccaro, R J -- Uyemura, K -- Cho, S -- Barnes, P F -- Rosat, J P -- Sette, A -- Brenner, M B -- Porcelli, S A -- Bloom, B R -- Modlin, R L -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1684-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California Los Angeles School of Medicine, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180075" target="_blank"〉PubMed〈/a〉
Keywords:
Antigens, CD1/*immunology
;
Antigens, CD95/immunology/metabolism
;
Cell Line
;
Coculture Techniques
;
Colony Count, Microbial
;
Cytoplasmic Granules/immunology
;
*Cytotoxicity, Immunologic
;
Fas Ligand Protein
;
Granzymes
;
Humans
;
Lymphocyte Activation
;
Macrophages/*immunology/microbiology
;
Membrane Glycoproteins/genetics/immunology/metabolism
;
Mycobacterium tuberculosis/growth & development/*immunology
;
Perforin
;
Phenotype
;
Pore Forming Cytotoxic Proteins
;
Serine Endopeptidases/metabolism
;
Strontium/pharmacology
;
T-Lymphocyte Subsets/*immunology
;
T-Lymphocytes, Cytotoxic/*immunology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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