Dallmann-Sauer Monica, Fava Vinicius M, Malherbe Stephanus T, MacDonald Candice E, Orlova Marianna, Kroon Elouise E, Cobat Aurélie, Boisson-Dupuis Stéphanie, Hoal Eileen G, Abel Laurent, Möller Marlo, Casanova Jean-Laurent, Walzl Gerhard, Du Plessis Nelita, Schurr Erwin
Program in Infectious Diseases and Immunity in Global Health, The Research Institute of the McGill University Health Centre, Montreal, Canada.
McGill International TB Centre, and.
J Clin Invest. 2025 Jan 21;135(7):e188016. doi: 10.1172/JCI188016.
BACKGROUNDNatural resistance to Mycobacterium tuberculosis (Mtb) infection in some people with HIV (PWH) is unexplained.METHODSWe performed single cell RNA-sequencing of bronchoalveolar lavage cells, unstimulated or ex vivo stimulated with Mtb, for 7 PWH who were tuberculin skin test (TST) and IFN-γ release assay (IGRA) positive (called LTBI) and 6 who were persistently TST and IGRA negative (called resisters).RESULTSAlveolar macrophages (AM) from resisters displayed a baseline M1 macrophage phenotype while AM from LTBI did not. Resisters displayed alveolar lymphocytosis, with enrichment of all T cell subpopulations including IFNG-expressing cells. In both groups, mycobactericidal granulysin was expressed almost exclusively by a T cell subtype that coexpressed granzyme B, perforin and NK cell receptors. These poly-cytotoxic T lymphocytes (poly-CTL) overexpressed activating NK cell receptors and were increased in resister BAL. Following challenge with Mtb, only intraepithelial lymphocyte-like cells from LTBI participants responded with increased transcription of IFNG. AM from resisters responded with a stronger TNF signature at 6 hours after infection while at 24 hours after infection, AM from LTBI displayed a stronger IFN-γ signature. Conversely, at 24 hours after infection, only AM from resisters displayed an upregulation of MHC class I polypeptide-related sequence A (MICA) transcripts, which encode an activating ligand for poly-CTL.CONCLUSIONThese results suggest that poly-CTL and M1-like pre-activated AM mediate the resister phenotype in PWH.FUNDINGNational Institutes of Health. Canadian Institutes of Health Research. Digital Research Alliance of Canada. French National Research Agency. French National Agency for Research on AIDS and Viral Hepatitis. St. Giles Foundation. General Atlantic Foundation. South African Medical Research Council Centre for Tuberculosis Research.
部分感染人类免疫缺陷病毒(HIV)的人(PWH)对结核分枝杆菌(Mtb)感染具有天然抵抗力,其原因尚不清楚。
我们对7名结核菌素皮肤试验(TST)和干扰素-γ释放试验(IGRA)呈阳性(称为潜伏性结核感染,LTBI)以及6名TST和IGRA持续呈阴性(称为抵抗者)的PWH的支气管肺泡灌洗细胞进行了单细胞RNA测序,这些细胞未受刺激或用Mtb进行体外刺激。
抵抗者的肺泡巨噬细胞(AM)呈现基线M1巨噬细胞表型,而LTBI者的AM则未呈现。抵抗者表现出肺泡淋巴细胞增多,包括表达IFNG的细胞在内的所有T细胞亚群均有富集。在两组中,几乎仅由共表达颗粒酶B、穿孔素和NK细胞受体的T细胞亚型表达杀分枝杆菌颗粒溶素。这些多细胞毒性T淋巴细胞(多CTL)过度表达激活NK细胞受体,且在抵抗者的支气管肺泡灌洗(BAL)中数量增加。在用Mtb攻击后,仅LTBI参与者的上皮内淋巴细胞样细胞IFNG转录增加。抵抗者的AM在感染后6小时以更强的TNF信号作出反应,而在感染后24小时,LTBI的AM表现出更强的IFN-γ信号。相反,在感染后24小时,只有抵抗者的AM显示出MHC I类多肽相关序列A(MICA)转录本上调,该转录本编码多CTL的激活配体。
这些结果表明,多CTL和M1样预激活的AM介导了PWH中的抵抗者表型。
美国国立卫生研究院。加拿大卫生研究院。加拿大数字研究联盟。法国国家研究机构。法国国家艾滋病和病毒性肝炎研究机构。圣贾尔斯基金会。泛大西洋基金会。南非医学研究理事会结核病研究中心。