Sustained IFN-I Expression during Established Persistent Viral Infection: A 'Bad Seed' for Protective Immunity
| Autor: | Alain Lamarre, Xavier Laulhé, Simona Stäger, Julien van Grevenynghe, Xavier Dagenais-Lussier, Hamza Loucif, Armstrong Murira |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
sustained IFN-I expression medicine.medical_treatment Clone (cell biology) lcsh:QR1-502 Review Receptor Interferon alpha-beta Biology Lymphocytic choriomeningitis medicine.disease_cause Antiviral Agents Virus lcsh:Microbiology Immune tolerance 03 medical and health sciences Immune system Virology exhaustion medicine Immune Tolerance Animals Humans immune activation/inflammation cell loss persistent infection immunosuppression Models Immunological Immunosuppression Simian immunodeficiency virus medicine.disease 030104 developmental biology Infectious Diseases Cytokine Virus Diseases Immunology Chronic Disease Interferon Type I IFNR blockade Signal Transduction |
| Zdroj: | Viruses Viruses, Vol 10, Iss 1, p 12 (2017) |
| ISSN: | 1999-4915 |
| Popis: | Type I interferons (IFN-I) are one of the primary immune defenses against viruses. Similar to all other molecular mechanisms that are central to eliciting protective immune responses, IFN-I expression is subject to homeostatic controls that regulate cytokine levels upon clearing the infection. However, in the case of established persistent viral infection, sustained elevation of IFN-I expression bears deleterious effects to the host and is today considered as the major driver of inflammation and immunosuppression. In fact, numerous emerging studies place sustained IFN-I expression as a common nexus in the pathogenesis of multiple chronic diseases including persistent infections with the human immunodeficiency virus type 1 (HIV-1), simian immunodeficiency virus (SIV), as well as the rodent-borne lymphocytic choriomeningitis virus clone 13 (LCMV clone 13). In this review, we highlight recent studies illustrating the molecular dysregulation and resultant cellular dysfunction in both innate and adaptive immune responses driven by sustained IFN-I expression. Here, we place particular emphasis on the efficacy of IFN-I receptor (IFNR) blockade towards improving immune responses against viral infections given the emerging therapeutic approach of blocking IFNR using neutralizing antibodies (Abs) in chronically infected patients. |
| Databáze: | OpenAIRE |
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