Abstract |
The evolution of Mycobacterium tuberculosis as an intracellular pathogen has led to a complex relationship between it and its host, the human mononuclear phagocyte. The products of M. tuberculosis-specific T lymphocytes are essential for macrophage activation for intracellular mycobacterial killing. However, dysfunction cell-mediated immune response to infection with M. tuberculosis may contribute to progressive primary infection or reactivation of endogenous foci of mycobacteria. Th1 cells produce IL-2, which is essential for proper cellular immunity. The aim of this study was to identify the variation in IL-2 activity and soluble IL-2 receptor (IL-2 R) in peripheral blood lymphocyte in patients suffering with pulmonary tuberculosis. A significant decrease in IL-2 and IL-2 receptor level was observed in patients with pulmonary tuberculosis when compared to normal controls. Our results suggested that patients with pulmonary tuberculosis had a defect in IL-2 production. Better understanding of these interactions will allow the development of increasingly specific immune-based interventions for prevention and treatment of tuberculosis.
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Authors | Madhu Khanna, L M Srivastava, Pankaj Kumar |
Journal | The Journal of communicable diseases
(J Commun Dis)
Vol. 35
Issue 2
Pg. 65-70
(Jun 2003)
ISSN: 0019-5138 [Print] India |
PMID | 15562950
(Publication Type: Journal Article)
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Chemical References |
- Interleukin-2
- Receptors, Interleukin-2
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Topics |
- Adolescent
- Adult
- Case-Control Studies
- Female
- Humans
- Interleukin-2
(biosynthesis)
- Leukocytes, Mononuclear
(metabolism)
- Male
- Middle Aged
- Receptors, Interleukin-2
(metabolism)
- Tuberculosis, Pulmonary
(blood, metabolism)
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