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Category: Bacterial Pathogenesis; Clinical Microbiology
Th1 and Th2 Cytokines in the Human Immune Response to Tuberculosis, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555817657/9781555812959_Chap31-1.gif /docserver/preview/fulltext/10.1128/9781555817657/9781555812959_Chap31-2.gifAbstract:
Immune defenses against Mycobacterium tuberculosis are mediated primarily by T cells, and IFN-γ is essential for protective immunity. Investigators have studied cytokine production and mRNA expression in bronchoalveolar lavage fluid and in lung tissue from patients with pulmonary tuberculosis, pleural fluid from those with tuberculous pleuritis, and lymph nodes from patients with tuberculous lymphadenitis. Most investigators have reported that peripheral blood mononuclear cells (PBMC) of tuberculosis patients show decreased Mycobacterium tuberculosis induced IFN-γ production. Helminthic infections and tuberculosis are both common in developing nations, and current or prior helminthic infections can strongly bias mycobacterial antigen-elicited cytokine production toward a Th2 response. Dysregulation of the systemic Th1 and Th2 cytokine responses may be a secondary effect of tuberculosis, since tuberculosis commonly results in malnutrition, which in turn is associated with enhanced Th2 and reduced Th1 cytokine responses. Local administration of cytokines is theoretically more appealing than systemic therapy, since the former approach is likely to result in fewer side effects.
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Cytokine production in human tuberculosis. At the tissue sites of disease, macrophages produce cytokines that favor the production of Th1 cells. Cytokines such as IL-10, IL-18, and IFN-γ leak into the systemic circulation, resulting in high levels in serum. In the blood, monocytes produce TGF-β and IL-10, which favor the development of Th2 cells, resulting in systemic production of IL-4. Elevated cortisol levels and helminthic infections probably contribute to these effects. M?, macrophage.
Cytokine production in human tuberculosis. At the tissue sites of disease, macrophages produce cytokines that favor the production of Th1 cells. Cytokines such as IL-10, IL-18, and IFN-γ leak into the systemic circulation, resulting in high levels in serum. In the blood, monocytes produce TGF-β and IL-10, which favor the development of Th2 cells, resulting in systemic production of IL-4. Elevated cortisol levels and helminthic infections probably contribute to these effects. M?, macrophage.