| Literature DB >> 33340449 |
Ekaterina Esaulova1, Shibali Das2, Dhiraj Kumar Singh3, Jose Alberto Choreño-Parra4, Amanda Swain1, Laura Arthur1, Javier Rangel-Moreno5, Mushtaq Ahmed2, Bindu Singh3, Ananya Gupta2, Luis Alejandro Fernández-López4, Maria de la Luz Garcia-Hernandez5, Allison Bucsan6, Chivonne Moodley6, Smriti Mehra6, Ethel García-Latorre7, Joaquin Zuniga8, Jeffrey Atkinson9, Deepak Kaushal10, Maxim N Artyomov11, Shabaana A Khader12.
Abstract
Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb) latently infects approximately one-fourth of the world's population. The immune mechanisms that govern progression from latent (LTBI) to active pulmonary TB (PTB) remain poorly defined. Experimentally Mtb-infected non-human primates (NHP) mirror the disease observed in humans and recapitulate both PTB and LTBI. We characterized the lung immune landscape in NHPs with LTBI and PTB using high-throughput technologies. Three defining features of PTB in macaque lungs include the influx of plasmacytoid dendritic cells (pDCs), an Interferon (IFN)-responsive macrophage population, and activated T cell responses. In contrast, a CD27+ Natural killer (NK) cell subset accumulated in the lungs of LTBI macaques. This NK cell population was also detected in the circulation of LTBI individuals. This comprehensive analysis of the lung immune landscape will improve the understanding of TB immunopathogenesis, providing potential targets for therapies and vaccines for TB control.Entities:
Keywords: NK cells; granulomas; immune protection; lung; pDCs; single cell technologies; tuberculosis; type I IFNs
Mesh:
Year: 2020 PMID: 33340449 PMCID: PMC7878437 DOI: 10.1016/j.chom.2020.11.013
Source DB: PubMed Journal: Cell Host Microbe ISSN: 1931-3128 Impact factor: 31.316