IL-17 and IL-22 production in HIV+ individuals with latent and active tuberculosis

BMC Infectious Diseases

Arunabala Chaudhury¹  Siva Sai Krovvidi²  Ramakrishna Vankayalapati³  Abhinav Van³  Vijaya Lakshmi Valluri⁴  Kamakshi Prudhula Devalraju⁴  Sharadambal Sunder Ramaseri⁴  Venkata Sanjeev Kumar Neela⁴ 

[1] Clinical Division, Cheyutha, LEPRA Society;Department of Biotechnology, Sreenidhi Institute of Science and Technology;Department of Pulmonary Immunology, Centre for Biomedical Research, University of Texas Health Centre;Immunology & Molecular Biology Department, Bhagwan Mahavir Medical Research Centre;

关键词: Human;    Latent tuberculosis;    HIV;    Cytokines;    IL-22;    IL-17;   

DOI  :  10.1186/s12879-018-3236-0

来源: DOAJ

【 摘 要 】

Abstract Background IL-17 and IL-22 cytokines play an important role in protective immune responses against Mycobacterium tuberculosis (Mtb) infection. Information on the production of these cytokines and the factors that regulate their production in the context of human immunodeficiency virus (HIV) and latent tuberculosis infection (LTBI) or active tuberculosis disease (ATB) is limited. In the current study, we compared the production of these two cytokines by PBMC of HIV-LTBI+ and HIV + LTBI+ individuals in response to Mtb antigens CFP-10 (culture filtrate protein) and ESAT-6 (Early Secretory Antigenic Target). We also determined the mechanisms involved in their production. Methods We cultured Peripheral Blood Mononuclear Cells (PBMCs) from HIV- individuals and HIV+ patients with latent tuberculosis and active disease with CFP-10 and ESAT-6. Production of IL-17, IL-22 and PD1 (Programmed Death 1), ICOS (Inducible T-cell Costimulator), IL-23R and FoxP3 (Forkhead box P3) expression on CD4+ T cells was measured. Results In response to Mtb antigens CFP-10 and ESAT-6, freshly isolated PBMCs from HIV+ LTBI+ and HIV+ active TB patients produced less IL-17 and IL-22 and more IL-10, expressed less IL-23R, and more PD1 and expanded to more FoxP3+ cells. Active TB infection in HIV+ individuals further inhibited antigen specific IL-17 and IL-22 production compared to those with LTBI. Neutralization of PD1 restored IL-23R expression, IL-17 and IL-22 levels and lowered IL-10 production and reduced expansion of FoxP3 T cells. Conclusions In the current study we found that increased PD1 expression in HIV + LTBI+ and HIV+ active TB patients inhibits IL-17, IL-22 production and IL-23R expression in response to Mtb antigens CFP-10 and ESAT-6.

【 授权许可】

Unknown