Infection and cancer suppress pDC derived IFN-I
| Autor: | Elina I. Zuniga, Trever T Greene, Yeara Jo |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Population Immunology Stimulation Infections Article 03 medical and health sciences 0302 clinical medicine Immunity Interferon Neoplasms medicine Immunology and Allergy 2.1 Biological and endogenous factors Humans Progenitor cell Aetiology education Receptor Cancer education.field_of_study business.industry Interferon-alpha hemic and immune systems Dendritic Cells medicine.disease 030104 developmental biology medicine.anatomical_structure Infectious Diseases Emerging Infectious Diseases 5.1 Pharmaceuticals Bone marrow Development of treatments and therapeutic interventions business 030215 immunology medicine.drug |
| Zdroj: | Curr Opin Immunol |
| Popis: | Plasmacytoid dendritic cells (pDCs) are specialized producers of Type I interferon (IFN-I) that promote anti-viral and anti-tumor immunity. However, chronic infections and cancer inhibit pDC-derived IFN-I. While the mechanisms of this inhibition are multifarious they can be classified broadly into two categories: i) reduction or ablation of pDC IFN-I-production capacity (functional exhaustion) and/or ii) decrease in pDC numbers (altered population dynamics). Recent work has identified many processes that contribute to suppression of pDC-derived IFN-I during chronic infections and cancer, including sustained stimulation through Toll Like Receptors (TLRs), inhibitory microenvironments, inhibitory receptor ligation, and reduced development from bone marrow progenitors and apoptosis. Emerging success leveraging pDCs in treatment of disease through TLR activation illustrates the therapeutic potential of targeting pDCs. Deeper understanding of the systems that limit pDC-derived IFN-I has the potential to improve these emerging therapies as well as help devising new approaches that harness the outstanding IFN-I-production capacity of pDCs. |
| Databáze: | OpenAIRE |
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