ReviewFrontiers in immunology2026
Mendelian susceptibility to mycobacterial disease: IFN-γ-driven immunity collapse underlies heterogeneous infections.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
7 authors.
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Abstract
Mendelian susceptibility to mycobacterial disease (MSMD) is a rare inborn error of immunity characterized by heightened susceptibility to low-virulence non-tuberculous mycobacteria. Despite the widespread application of next-generation sequencing, the molecular etiology of approximately 50% of patients remains elusive. To date, 22 genes have been implicated, all converging on the IL-12/23-IFN-γ circuit, underscoring its non-redundant role in controlling intracellular pathogens. Isolated MSMD is characterized by a selective predisposition to one or more mycobacterial and related infections. But syndromic MSMD's clinical phenotypes are highly heterogeneous; apart from mycobacterial infections, patients may suffer from viral, bacterial, or fungal diseases, and can additionally manifest auto-inflammation, malignancy, or cutaneous involvement. Current MSMD management mainly hinges on prolonged antimicrobial therapy or align with recombinant human interferon-γ (rhIFN-γ), although allogeneic hematopoietic stem cell transplantation (HSCT) remains the sole curative yet high-risk option; gene editing is still experimental. Priorities are early high-risk identification, targeted intervention and full-process management.
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