期刊
CYTOKINE
卷 49, 期 2, 页码 171-176出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2009.10.003
关键词
Cytokines; Endotoxin/LPS; Inflammation; Macrophages/monocytes; Arthritis/rheumatoidarthritis
资金
- Korea Government (MOST) [R01-2006-000-10837]
- Korea Science and Engineering Foundation [R01-2006-000-10145-0]
- Korea Research Foundation
- Ministry of Knowledge Economy
- National Research Foundation of Korea [R01-2006-000-10837-0, R01-2006-000-10145-0, 313-2008-2-C00644] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Targeting major proinflammatory cytokines such as IL-1 beta and TNF alpha is of great interest in patients with chronic inflammatory diseases, including rheumatoid arthritis, colitis, and psoriasis. The cytokine Interleukin (IL)-32 induces proinflammatory cytokines such as TNF alpha, IL-1 beta. IL-6, and chemokines. We previously used an IL-32 ligand-affinity column to purify proteinase 3, which is abundantly expressed in neutrophil and monocytic leukocytes but not in other cell types, and found that IL-32 is mainly produced by monocytic leukocytes. This evidence suggested that silencing endogenous IL-32 by short hairpin RNA (shRNA) in monocytic cells might reveal the precise function of endogenous IL-32. Indeed, lipopolysaccharide (LPS)- or phorbol myristate acetate (PMA)-induced proinflammatory cytokine production was significantly inhibited in shRNA/IL-32 stable clones as compared to control clones. Furthermore, macrophages in PMA-differentiated shRNA/IL-32 stable clones displayed remarkably impaired LPS- and IL-1 beta-induced proinflammatory cytokine production. These data suggest that IL-32 is not only involved in host defense against pathogens, but also might play a role in chronic inflammatory diseases. IL-32 production leads to major proinflammatory cytokine production during the initial immune response. (C) 2009 Published by Elsevier Ltd.
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