Interleukin-34 Promotes Fibrocyte Proliferation
Autor: | Carole L. Galligan, Eleanor N. Fish |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Male Pluripotent Stem Cells Immunology Arthritis Gene Expression Enzyme-Linked Immunosorbent Assay Pathogenesis Arthritis Rheumatoid 03 medical and health sciences Mice 0302 clinical medicine Virology Fibrocyte medicine Synovial fluid Rheumatoid factor Animals Humans Cell Proliferation 030203 arthritis & rheumatology business.industry Interleukins Mesenchymal stem cell Mesenchymal Stem Cells Cell Biology medicine.disease Arthritis Experimental Immunohistochemistry Disease Models Animal 030104 developmental biology Rheumatoid arthritis Interleukin 34 business Biomarkers |
Zdroj: | Journal of interferoncytokine research : the official journal of the International Society for Interferon and Cytokine Research. 37(10) |
ISSN: | 1557-7465 |
Popis: | Rheumatoid arthritis (RA) is a systemic autoimmune disease affecting multiple joints. It remains unclear which factors in the circulation are associated with the systemic spread of the disease. Fibrocytes are pluripotent mesenchymal stem cells present in the circulation of RA patients. Our earlier findings implicated activated fibrocytes in the etiology of onset and pathogenesis of RA. Elevated levels of interleukin-34 (IL-34) in the serum and synovial fluid of RA patients are associated with rheumatoid factor and anticyclic citrullinated peptide antibodies, indicators of RA. Moreover, IL-34 levels are independent predictors of radiographic progression in RA patients. We provide evidence of simultaneous elevated levels of IL-34 and increased numbers of activated fibrocytes in the circulation of mice induced to develop arthritis. In vitro, IL-34 treatment induced the proliferation of fibrocytes, mediated by activation of cognate CSF-R1s on fibrocytes. Taken together, we infer that IL-34 has a role in stimulating fibrocyte proliferation and activation during arthritis, thereby contributing to both onset of RA and systemic spread of disease. |
Databáze: | OpenAIRE |
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