Short-term IL-1beta blockade reduces monocyte CD11b integrin expression in an IL-8 dependent fashion in patients with type 1 diabetes
Cytokines;Chemokines;细胞因子;趋化因子;MSD;Cytokines;Chemokines- Clin Immunol.
- 2010
- 136(2):170-3.
- Human,Mouse,Non-Human Primate,Rat
- MSD
- Serum
- 免疫/内分泌
- 单核细胞
- 糖尿病
- CRP, IL-10, IL-12 p70, IL-17A, IL-2, IL-4, IL-5, IL-6, IL-8, MCP-1
相关货号
LXMH04-4LXMH06-1LXMH07-4LXMH09-1LXMH09-2LXMH10-8LXMH111-1LXMM10-4LXMN03-1LXMN05-1LXMN06-3
Abstract
Objective: Interleukin 1-beta (IL-1beta) is a major inflammatory cytokine. Blockade of the IL-1beta pathway is therapeutically efficacious in type 2 diabetes, but the mechanistic effects on the immune system are incompletely understood.
Research design: We administered an IL-1 receptor antagonist, anakinra, to 7 type 1 diabetes patients in order to investigate the immunologic and metabolic effects of this drug. Mechanistic assays were performed before and after drug administration.
Results: A novel signature was observed, with reduced serum interleukin 8 (IL-8) levels and reduced CD11b integrin expression on monocytes associated with increased CXCR1 expression.
Conclusions: This set of linked phenotypes suggests that blockade of the IL-1beta pathway results in the reduced ability of mononuclear cells to traffic to sites of inflammation. Mechanistic studies from large scale trials using IL-1 blockade in type 1 diabetes should focus on changes in monocyte trafficking and the IL-8 pathway.
Research design: We administered an IL-1 receptor antagonist, anakinra, to 7 type 1 diabetes patients in order to investigate the immunologic and metabolic effects of this drug. Mechanistic assays were performed before and after drug administration.
Results: A novel signature was observed, with reduced serum interleukin 8 (IL-8) levels and reduced CD11b integrin expression on monocytes associated with increased CXCR1 expression.
Conclusions: This set of linked phenotypes suggests that blockade of the IL-1beta pathway results in the reduced ability of mononuclear cells to traffic to sites of inflammation. Mechanistic studies from large scale trials using IL-1 blockade in type 1 diabetes should focus on changes in monocyte trafficking and the IL-8 pathway.
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