Impaired M. tuberculosis-mediated apoptosis in alveolar macrophages from HIV+ persons: potential role of IL-10 and BCL-3

• Published in: Journal of leukocyte biology Vol. 86; no. 1; pp. 53 - 60
• Main Authors: Patel, Naimish R., Swan, Katharine, Li, Xin, Tachado, Souvenir D., Koziel, Henry
• Format: Journal Article
• Language: English
• Published: United States Society for Leukocyte Biology 01.07.2009; The Society for Leukocyte Biology
• Subjects: Alveoli; Apoptosis; Apoptosis - immunology; Bcl-3 protein; Data processing; Disease Susceptibility; HIV Infections - complications; Human immunodeficiency virus; Humans; Immunity, Innate; Interleukin 10; Interleukin-10 - analysis; Interleukin-10 - physiology; Leukocytes; Lung; Lung - chemistry; Macrophages; Macrophages, Alveolar - immunology; Macrophages, Alveolar - microbiology; Macrophages, Alveolar - virology; molecules; mRNA; NF-kappa B - antagonists & inhibitors; NF‐κB; Nuclear transport; Proto-Oncogene Proteins - analysis; Proto-Oncogene Proteins - physiology; Spotlight on Leading Edge Research; Toll‐like receptors; transcription factors; Transcription Factors - analysis; Transcription Factors - physiology; Tuberculosis - etiology; Tuberculosis - pathology; Tuberculosis - virology; Tumor necrosis factor

HIV alters the lung environment through increased IL‐10, leading to an impaired macrophage apoptotic response to Mycobacterium tuberculosis via upregulation of macrophage BCL‐3. The mechanism of increased MTb disease susceptibility in HIV+ persons remains poorly understood. Apoptosis of macrophages...