The light and the dark sides of Interleukin-10 in immune-mediated diseases and cancer
| Autor: | Pier Luigi Meroni, Richard A. Flavell, Moira Paroni, Sergio Abrignani, Giulia Nizzoli, Jens Geginat, A.E. Penatti, Nicola Gagliani, Paola Larghi, Massimiliano Pagani |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Endocrinology Diabetes and Metabolism medicine.medical_treatment T cell T-Lymphocytes Immunology Biology General Biochemistry Genetics and Molecular Biology 03 medical and health sciences Immune system Neoplasms medicine Immunology and Allergy Cytotoxic T cell Animals Homeostasis Humans Lupus Erythematosus Systemic Colitis B-Lymphocytes Cancer medicine.disease Interleukin-10 Intestines CTL Interleukin 10 030104 developmental biology Cytokine medicine.anatomical_structure |
| Zdroj: | Cytokinegrowth factor reviews. 30 |
| ISSN: | 1879-0305 |
| Popis: | Interleukin-10 (IL-10) is known to be a tolerogenic cytokine since it inhibits pro-inflammatory cytokine production and T cell stimulatory capacities of myeloid cells, such as macrophages and dendritic cells. In particular, it has a non-redundant tolerogenic role in intestinal immune homeostasis, since mice and patients with genetic defects in the IL-10/IL-10R pathway develop spontaneously colitis in the presence of a normal intestinal flora. However, IL-10 is also a growth and differentiation factor for B-cells, can promote autoantibody production and has consequently a pathogenic role in systemic lupus erythematosus. Moreover, IL-10 can promote cytotoxic T-cell (CTL) responses and this immunogenic activity might be relevant in type-1 diabetes and anti-tumor immune responses. This review summarizes these paradoxic effects of IL-10 on different types of immune responses, and proposes that different cellular sources of IL-10, in particular IL-10-secreting helper and regulatory T-cells, have different effects on B-cell and CTL responses. Based on this concept we discuss the rationales for targeting the IL-10 pathway in immune-mediated diseases and cancer. |
| Databáze: | OpenAIRE |
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