ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Molecular and cellular mechanisms of Mycobacterium avium-induced thymic atrophy.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Depletion of myeloid cells in AG129 mice reduces the infection-mediated oxidative stress and restrains dengue virus-induced thymic atrophy.Cell communication and signaling : CCS · 2025Article
- Endogenous thymic regeneration: restoring T cell production following injury.Nature reviews. Immunology · 2025Review
- SARS-CoV-2 variants induce distinct disease and impact in the bone marrow and thymus of mice.iScience · 2023Article
- Thymus, undernutrition, and infection: Approaching cellular and molecular interactions.Frontiers in nutrition · 2022Review
- IFNγ and iNOS-Mediated Alterations in the Bone Marrow and Thymus and Its Impact onFrontiers in immunology · 2021Article
- Infection-Associated Thymic Atrophy.Frontiers in immunology · 2021Review
- The Teleost Thymus in Health and Disease: New Insights from Transcriptomic and Histopathological Analyses of Turbot,Biology · 2020Article
- Streptococcus suis Serotype 2 Infection Causes Host Immunomodulation through Induction of Thymic Atrophy.Infection and immunity · 2020Article
- Article
- Construction of Thymus Organoids from Decellularized Thymus Scaffolds.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Tuberculosis, the Disrupted Immune-Endocrine Response and the Potential Thymic Repercussion As a Contributing Factor to Disease Physiopathology.Frontiers in endocrinology · 2018Review
- Differential susceptibility and maturation of thymocyte subsets during Salmonella Typhimurium infection: insights on the roles of glucocorticoids and Interferon-gamma.Scientific reports · 2017Article
- Systemic toxoplasma infection triggers a long-term defect in the generation and function of naive T lymphocytes.The Journal of experimental medicine · 2016Article
- Airway delivery of interferon-γ overexpressing macrophages confers resistance to Mycobacterium avium infection in SCID mice.Physiological reports · 2016Article
- Activation of the hypothalamic-pituitary-adrenal (HPA) axis contributes to the immunosuppression of mice infected with Angiostrongylus cantonensis.Journal of neuroinflammation · 2016Article
- Severe influenza A(H1N1)pdm09 infection induces thymic atrophy through activating innate CD8(+)CD44(hi) T cells by upregulating IFN-γ.Cell death & disease · 2014Article
- Tolerance has its limits: how the thymus copes with infection.Trends in immunology · 2013Review
- T cells home to the thymus and control infection.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 4 countries.
Funding
Abstract
Thymic atrophy has been described as a consequence of infection by several pathogens and shown to be induced through diverse mechanisms. Using the mouse model of Mycobacterium avium infection, we show in this study that the production of NO from IFN-γ-activated macrophages plays a major role in mycobacterial infection-induced thymic atrophy. Our results show that disseminated infection with a highly virulent strain of M. avium, but not with a low-virulence strain, led to a progressive thymic atrophy. Thymic involution was prevented in genetically manipulated mice unable to produce IFN-γ or the inducible NO synthase. In addition, mice with a selective impairment of IFN-γ signaling in macrophages were similarly protected from infection-induced thymic atrophy. A slight increase in the concentration of corticosterone was found in mice infected with the highly virulent strain, and thymocytes presented an increased susceptibility to dexamethasone-induced death during disseminated infection. The administration of an antagonist of glucocorticoid receptors partially reverted the infection-induced thymic atrophy. We observed a reduction in all thymocyte populations analyzed, including the earliest thymic precursors, suggesting a defect during thymic colonization by T cell precursors and/or during the differentiation of these cells in the bone marrow in addition to local demise of thymic cells. Our data suggest a complex picture underlying thymic atrophy during infection by M. avium with the participation of locally produced NO, endogenous corticosteroid activity, and reduced bone marrow seeding.
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Registered trials
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