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α1-Antitrypsin inhibits Moraxella catarrhalis MID protein-induced tonsillar B cell proliferation and IL-6 release
Malmö University Hospital.
Malmö University Hospital.
Malmö University Hospital.ORCID-id: 0000-0003-4190-5431
Malmö University Hospital.
Vise andre og tillknytning
2006 (engelsk)Inngår i: Immunology Letters, ISSN 0165-2478, E-ISSN 1879-0542, Vol. 102, nr 2, s. 141-147Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

α1-Antitrypsin (AAT) is a major circulating and tissues inhibitor of serine proteinases implicated in the regulation of inflammation and host defence. There is now increasing evidence that AAT may also exhibit anti-inflammatory activities independent of its protease inhibitor function. This study was undertaken to investigate the effects of native (inhibitory) and polymerized (non-inhibitory) forms of AAT on MID (Moraxella IgD binding protein)-induced human tonsillar B cell activation in vitro. We found that 0.5 μg/ml MID induces B cell proliferation and stimulates IL-6 release (p < 0.001) relative to non-stimulated controls. Both native and polymerized AAT (0.5 mg/ml) inhibited MID-stimulated B cell proliferation in a similar manner (by 70%, p < 0.001), whereas MID-induced IL-6 release was more strongly suppressed by polymerized (9.9-fold, p < 0.001) as compared to native AAT (2.8-fold, p < 0.01). Electrophoretic analysis of cell culture media did not indicate any interaction between AAT and MID, and flow cytometry data showed no competition for the same receptor. The effects of AATs were observed whether added together with MID or 2 h after MID-addition to cell cultures. Thus, our data demonstrate that AAT inhibits MID-induced B cell activation in vitro that is unrelated to its protease inhibitory activity and is not dependent on MID binding to the cell surface.

sted, utgiver, år, opplag, sider
2006. Vol. 102, nr 2, s. 141-147
Emneord [en]
α1-Antitrypsin, tonsils, B cells, Inflammation, MID
HSV kategori
Identifikatorer
URN: urn:nbn:se:hkr:diva-15681DOI: 10.1016/j.imlet.2005.08.006PubMedID: 16214222OAI: oai:DiVA.org:hkr-15681DiVA, id: diva2:952023
Forskningsfinansiär
The Crafoord FoundationTilgjengelig fra: 2016-08-11 Laget: 2016-08-11 Sist oppdatert: 2017-11-28bibliografisk kontrollert

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