Gliadin peptides activate blood monocytes from patients with celiac disease
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem, Research Support, U.S. Gov't, Non-P.H.S.
Grantová podpora
DK-064400
NIDDK NIH HHS - United States
DK-47322
NIDDK NIH HHS - United States
DK-54495
NIDDK NIH HHS - United States
DK-74033
NIDDK NIH HHS - United States
HD-41361
NICHD NIH HHS - United States
- MeSH
- aktivace makrofágů imunologie MeSH
- antigen CD83 MeSH
- antigeny CD40 metabolismus MeSH
- antigeny CD80 metabolismus MeSH
- antigeny CD86 metabolismus MeSH
- CD antigeny metabolismus MeSH
- celiakie imunologie metabolismus MeSH
- cytokiny biosyntéza MeSH
- gliadin metabolismus MeSH
- HLA-DQ antigeny metabolismus MeSH
- imunoglobuliny metabolismus MeSH
- interleukin-8 biosyntéza MeSH
- lidé MeSH
- membránové glykoproteiny metabolismus MeSH
- monocyty metabolismus MeSH
- NF-kappa B metabolismus MeSH
- peptidové fragmenty MeSH
- průtoková cytometrie MeSH
- TNF-alfa biosyntéza MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
- Research Support, U.S. Gov't, Non-P.H.S. MeSH
- Názvy látek
- antigeny CD40 MeSH
- antigeny CD80 MeSH
- antigeny CD86 MeSH
- CD antigeny MeSH
- cytokiny MeSH
- gliadin MeSH
- HLA-DQ antigeny MeSH
- HLA-DQ2 antigen MeSH Prohlížeč
- imunoglobuliny MeSH
- interleukin-8 MeSH
- membránové glykoproteiny MeSH
- NF-kappa B MeSH
- peptidové fragmenty MeSH
- TNF-alfa MeSH
To elucidate the role of innate immune responses in celiac disease, we investigated the effect of gliadin on blood monocytes from patients with celiac disease. Gliadin induced substantial TNF-alpha and IL-8 production by monocytes from patients with active celiac disease, lower levels by monocytes from patients with inactive celiac disease, and even lower levels by monocytes from healthy donors. In healthy donor monocytes gliadin induced IL-8 from monocytes expressing HLA-DQ2 and increased monocyte expression of the costimulatory molecules CD80 and CD86, the dendritic cell marker CD83, and the activation marker CD40. Gliadin also increased DNA binding activity of NF-kappaB p50 and p65 subunits in monocytes from celiac patients, and NF-kappaB inhibitors reduced both DNA binding activity and cytokine production. Thus, gliadin activation of HLA-DQ2(+) monocytes leading to chemokine and proinflammatory cytokine production may contribute to the host innate immune response in celiac disease.
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