Universidad Peruana Cayetano Heredia

T-cell deficiency and hyperinflammatory monocyte responses associate with Mycobacterium avium complex lung disease

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dc.contributor.author Lindestam Arlehamn, C.S.
dc.contributor.author Benson, B.
dc.contributor.author Kuan, R.
dc.contributor.author Dill-McFarland, K.A.
dc.contributor.author Peterson, G.J.
dc.contributor.author Paul, S.
dc.contributor.author Nguyen, F.K.
dc.contributor.author Gilman, Robert Hugh
dc.contributor.author Saito, M.
dc.contributor.author Taplitz, R.
dc.contributor.author Arentz, M.
dc.contributor.author Goss, C.H.
dc.contributor.author Aitken, M.L.
dc.contributor.author Horne, D.J.
dc.contributor.author Shah, J.A.
dc.contributor.author Sette, A.
dc.contributor.author Hawn, T.R.
dc.date.accessioned 2022-11-15T23:04:40Z
dc.date.available 2022-11-15T23:04:40Z
dc.date.issued 2022
dc.identifier.uri https://hdl.handle.net/20.500.12866/12581
dc.description.abstract Immunological mechanisms of susceptibility to nontuberculous mycobacterial (NTM) disease are poorly understood. To understand NTM pathogenesis, we evaluated innate and antigen-specific adaptive immune responses to Mycobacterium avium complex (MAC) in asymptomatic individuals with a previous history of MAC lung disease (MACDZ). We hypothesized that Mav-specific immune responses are associated with susceptibility to MAC lung disease. We measured MAC-, NTM-, or MAC/Mtb-specific T-cell responses by cytokine production, expression of surface markers, and analysis of global gene expression in 27 MACDZ individuals and 32 healthy controls. We also analyzed global gene expression in Mycobacterium avium-infected and uninfected peripheral blood monocytes from 17 MACDZ and 17 healthy controls. We were unable to detect increased T-cell responses against MAC-specific reagents in MACDZ compared to controls, while the responses to non-mycobacteria derived antigens were preserved. MACDZ individuals had a lower frequency of Th1 and Th1* T-cell populations. In addition, MACDZ subjects had lower transcriptional responses in PBMCs stimulated with a mycobacterial peptide pool (MTB300). By contrast, global gene expression analysis demonstrated upregulation of proinflammatory pathways in uninfected and M. avium-infected monocytes, i.e. a hyperinflammatory in vitro response, derived from MACDZ subjects compared to controls. Together, these data suggest a novel immunologic defect which underlies MAC pathogenesis and includes concurrent innate and adaptive dysregulation which persists years after completion of treatment. en_US
dc.language.iso eng
dc.publisher Frontiers Media
dc.relation.ispartofseries Frontiers in Immunology
dc.rights info:eu-repo/semantics/restrictedAccess
dc.rights.uri https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
dc.subject mycobacterium avium complex en_US
dc.subject MAC en_US
dc.subject NTM = nontuberculous mycobacteria en_US
dc.subject immune response en_US
dc.subject MAC pathogenesis en_US
dc.subject T cells en_US
dc.title T-cell deficiency and hyperinflammatory monocyte responses associate with Mycobacterium avium complex lung disease en_US
dc.type info:eu-repo/semantics/article
dc.identifier.doi https://doi.org/10.3389/fimmu.2022.1016038
dc.relation.issn 1664-3224


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