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REVIEW ARTICLE

Comparison of immune evasion mechanisms of multidrug-resistant Mycobacterium tuberculosis versus nontuberculous mycobacteria

Nazmun Nahar1 ,  Redwana Jannat1 ,  Shefa Mannan Nuha1 ,  Md. Fakruddin1*
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1 Department of Microbiology, School of Health & Life Sciences, North South University, Dhaka, Dhaka Division, Bangladesh
MI, 026210052 https://doi.org/10.36922/MI026210052
Received: 22 May 2026 | Revised: 22 June 2026 | Accepted: 1 July 2026 | Published online: 22 July 2026
© 2026 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )
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Abstract

Mycobacterium tuberculosis (MTB) and nontuberculous mycobacteria (NTM) are important worldwide health problems because they may challenge human immunity and cause chronic infections. This study presents a comparative overview of immune evasion mechanisms in multidrug-resistant MTB (MDR-MTB) and NTM, focusing on mechanisms supported by direct experimental evidence and those inferred from drug-susceptible MTB. Supported findings in MDR-MTB include LAM-mediated block of phagolysosomal fusion, depletion of PI3P by SapM, and Zmp1-mediated suppression of AIM2 inflammasome activation. Mutations in katG and rpoB confer resistance to isoniazid and rifampicin. However, these primarily affect drug susceptibility rather than immune modulation. Other processes, such as ESX-1–mediated membrane disruption, PPE protein interference with oxidative stress, and ubiquitination pathway evasion, are well described in drug-susceptible MTB and are inferred to contribute to MDR-MTB persistence. For NTM, experimental evidence demonstrates immune evasion through biofilm formation (glycopeptidolipids, PKS1, polyphosphate accumulation), active efflux pumps, and cytokine modulation via LAM and Toll-like receptor 2 (TLR2) blockade. NTM also inhibits phagolysosomal fusion using SapM and PtpA, while granuloma formation sustains long-term infection. Both bacteria use overlapping mechanisms, including inhibition of phagosome-lysosome fusion, modulation of cytokine responses, and granuloma formation, but differ in their ecological niches, transmission, and clinical presentations. These immune-evasive features complicate therapy, prolong treatment, and hamper vaccine development. Emerging therapeutics include autophagy inducers (e.g., rapamycin) and host-directed therapies (e.g., interferon-gamma). Future prospects include personalized medicine, innovative vaccination platforms such as messenger RNA-based techniques, and a One Health approach to address the interconnected issues of MDR-MTB and NTM. Thus, this review explicitly distinguishes experimentally validated immune evasion mechanisms underlying MDR-MTB from those extrapolated from drug-susceptible strains, while integrating evidence-based findings for NTM.

Graphical abstract
Keywords
Multidrug-resistant Mycobacterium tuberculosis
Nontuberculous mycobacteria
Immune evasion mechanisms
Phagosome–lysosome fusion inhibition
Biofilm persistence
Host-directed therapies
Funding
None.
Conflict of interest
The authors declare they have no competing interests.
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Microbes & Immunity, Electronic ISSN: 3029-2883 Print ISSN: 3041-0886, Published by AccScience Publishing
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