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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Adaptive Immunity, Adolescent, Adult, Antigens, Bacterial, CD3 Complex, CD4-Positive T-Lymphocytes, CD56 Antigen, CD8-Positive T-Lymphocytes, Female, HIV Infections, Humans, Immunity, Innate, Interferon-gamma, Interleukin-10, Interleukin-4, Male, Mycobacterium tuberculosis, Young Adult.
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Does hIV Progression perturb the Balance of the Cell-Mediated and Anti-Inflammatory Adaptive and Innate Mycobacterial Immune Response? Context: Our objective is to understand how HIV infection increases the risk of progression from latent tuberculosis (TB) to active disease. We understand now that immunity is a balance of competing immune responses by multiple cell types. Since T-lymphocyte production of interferon-gamma (IFN-γ) in response to Mycobacterium tuberculosis (Mtb) antigens fails to differentiate disease from latent infection, we applied a comprehensive profiling methodology to define immune biomarkers that reliably predict a patient's TB risk. We established a cohort of HIV-infected adults with TB disease from Swaziland. Multiparametric flow cytometry was used to quantify the mycobacterial-specific anti-inflammatory (IL-4 and IL-10) and proinflammatory (IFN-γ) immune response. From 12 HIV-infected Swaziland patients with TB disease, the CD4(+), CD8(+), Double Negative, and CD56(+)CD3(-) lymphocytes increase their IL-4 : IFN-γ ratio as HIV disease worsens (Spearman r of -0.59; -0.59; -0.60; and -0.59, resp.; p < 0.05). Similarly, HIV severity is associated with an increased IL-10 : IFN-γ ratio (Spearman r of -0.76; p = 0.01).
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As HIV disease progresses, both the adaptive and innate branches skew away from an inflammatory and towards anti-inflammatory phenotype. Final Decision: yes