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Merck
  • The immune landscape in tuberculosis reveals populations linked to disease and latency.

The immune landscape in tuberculosis reveals populations linked to disease and latency.

Cell host & microbe (2020-12-20)
Ekaterina Esaulova, Shibali Das, Dhiraj Kumar Singh, Jose Alberto Choreño-Parra, Amanda Swain, Laura Arthur, Javier Rangel-Moreno, Mushtaq Ahmed, Bindu Singh, Ananya Gupta, Luis Alejandro Fernández-López, Maria de la Luz Garcia-Hernandez, Allison Bucsan, Chivonne Moodley, Smriti Mehra, Ethel García-Latorre, Joaquin Zuniga, Jeffrey Atkinson, Deepak Kaushal, Maxim N Artyomov, Shabaana A Khader
초록

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.

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Sigma-Aldrich
Anti-IDO1 antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
Sigma-Aldrich
Anti-ROR gamma T Antibody, clone 6F3.1, clone 6F3.1, from mouse