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Induction of thymic atrophy and loss of thymic output by type-I interferons during chronic viral infection.
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- Author(s): Démoulins T;Démoulins T;Démoulins T; Baron ML; Baron ML; Gauchat D; Gauchat D; Kettaf N; Kettaf N; Reed SJ; Reed SJ; Charpentier T; Charpentier T; Kalinke U; Kalinke U; Lamarre A; Lamarre A; Ahmed R; Ahmed R; Sékaly RP; Sékaly RP; Sarkar S; Sarkar S; Sarkar S; Sarkar S; Kalia V; Kalia V; Kalia V
- Source:
Virology [Virology] 2022 Feb; Vol. 567, pp. 77-86. Date of Electronic Publication: 2021 Dec 24.- Publication Type:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't- Language:
English - Source:
- Additional Information
- Source: Publisher: Academic Press Country of Publication: United States NLM ID: 0110674 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1096-0341 (Electronic) Linking ISSN: 00426822 NLM ISO Abbreviation: Virology Subsets: MEDLINE
- Publication Information: Original Publication: New York, Academic Press.
- Subject Terms: Atrophy/*virology ; Interferon-alpha/*immunology ; Interferon-beta/*immunology ; Lymphocytic Choriomeningitis/*virology ; Lymphocytic choriomeningitis virus/*immunology ; Thymocytes/*virology ; Thymus Gland/*virology; Animals ; Atrophy/genetics ; Atrophy/immunology ; Atrophy/pathology ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/virology ; Chronic Disease ; Female ; Gene Expression Regulation ; Humans ; Immunologic Memory ; Interferon-alpha/genetics ; Interferon-beta/genetics ; Lymph Nodes/immunology ; Lymph Nodes/pathology ; Lymph Nodes/virology ; Lymphocyte Depletion ; Lymphocytic Choriomeningitis/genetics ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic Choriomeningitis/pathology ; Lymphocytic choriomeningitis virus/pathogenicity ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Receptor, Interferon alpha-beta/deficiency ; Receptor, Interferon alpha-beta/genetics ; Receptor, Interferon alpha-beta/immunology ; Signal Transduction/immunology ; Single-Cell Analysis ; Thymocytes/immunology ; Thymocytes/pathology ; Thymus Gland/immunology ; Thymus Gland/pathology
- Abstract: Type-I interferon (IFN-I) signals exert a critical role in disease progression during viral infections. However, the immunomodulatory mechanisms by which IFN-I dictates disease outcomes remain to be fully defined. Here we report that IFN-I signals mediate thymic atrophy in viral infections, with more severe and prolonged loss of thymic output and unique kinetics and subtypes of IFN-α/β expression in chronic infection compared to acute infection. Loss of thymic output was linked to inhibition of early stages of thymopoiesis (DN1-DN2 transition, and DN3 proliferation) and pronounced apoptosis during the late DP stage. Notably, infection-associated thymic defects were largely abrogated upon ablation of IFNαβR and partially mitigated in the absence of CD8 T cells, thus implicating direct as well as indirect effects of IFN-I on thymocytes. These findings provide mechanistic underpinnings for immunotherapeutic strategies targeting IFN-1 signals to manipulate disease outcomes during chronic infections and cancers.
(Copyright © 2021. Published by Elsevier Inc.) - Grant Information: R21 AI154363 United States AI NIAID NIH HHS; R03 AI103748 United States AI NIAID NIH HHS; R01 AI132819 United States AI NIAID NIH HHS
- Contributed Indexing: Keywords: Acute; CD8 T cells; Chronic; Thymic atrophy; Thymopoiesis; Type-I interferons; Viral infection
- Accession Number: 0 (Interferon-alpha)
156986-95-7 (Receptor, Interferon alpha-beta)
77238-31-4 (Interferon-beta) - Publication Date: Date Created: 20220115 Date Completed: 20220217 Latest Revision: 20230129
- Publication Date: 20240105
- Accession Number: 10.1016/j.virol.2021.12.007
- Accession Number: 35032866
- Source:
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