Lymphocytic choriomeningitis virus Clone 13 infection causes either persistence or acute death dependent on IFN-1, cytotoxic T lymphocytes (CTLs), and host genetics
| Autor: | Megan J. Welch, Zaverio M. Ruggeri, Lucy E Horton, Roberto Aiolfi, Brian M. Sullivan, Brian C. Ware, Alessandro Zarpellon, Michael B. A. Oldstone |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
LAG3 T cell Programmed Cell Death 1 Receptor Clone (cell biology) Biology CD8-Positive T-Lymphocytes Lymphocytic Choriomeningitis Lymphocytic choriomeningitis Virus Replication Virus Pathogenesis 03 medical and health sciences Mice Antigens CD medicine Cytotoxic T cell Animals Humans Lymphocytic choriomeningitis virus Multidisciplinary medicine.disease Virology Lymphocyte Activation Gene 3 Protein 030104 developmental biology medicine.anatomical_structure Viral replication PNAS Plus Interferon Type I |
| Zdroj: | Proceedings of the National Academy of Sciences of the United States of America. 115(33) |
| ISSN: | 1091-6490 |
| Popis: | Understanding of T cell exhaustion and successful therapy to restore T cell function was first described using Clone (Cl) 13 variant selected from the lymphocytic choriomeningitis virus (LCMV) Armstrong (ARM) 53b parental strain. T cell exhaustion plays a pivotal role in both persistent infections and cancers of mice and humans. C57BL/6, BALB, SWR/J, A/J, 129, C3H, and all but one collaborative cross (CC) mouse strain following Cl 13 infection have immunosuppressed T cell responses, high PD-1, and viral titers leading to persistent infection and normal life spans. In contrast, the profile of FVB/N, NZB, PL/J, SL/J, and CC NZO mice challenged with Cl 13 is a robust T cell response, high titers of virus, PD-1, and Lag3 markers on T cells. These mice all die 7 to 9 d after Cl 13 infection. Death is due to enhanced pulmonary endothelial vascular permeability, pulmonary edema, collapse of alveolar air spaces, and respiratory failure. Pathogenesis involves abundant levels of Cl 13 receptor alpha-dystroglycan on endothelial cells, with high viral replication in such cells leading to immunopathologic injury. Death is aborted by blockade of interferon-1 (IFN-1) signaling or deletion of CD8 T cells. |
| Databáze: | OpenAIRE |
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