ArticleRheumatology international2008
Modulation of the Fcgamma receptors induced by anti-Ro and anti-La autoantibodies: observations in salivary gland cells.
Article in Rheumatology international, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 11 citations in OpenAlex.
- Rituximab-mediated Raf kinase inhibitor protein induction modulates NF-κB in Sjögren syndrome.Immunology · 2014Article
- Salivary gland expression level of IκBα regulatory protein in Sjögren's syndrome.Journal of molecular histology · 2013Article
- Advances in the understanding of the Fc gamma receptors-mediated autoantibodies uptake.Clinical and experimental medicine · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Only few reports have shown protein expression of the Fcgamma receptors (FcgammaRs) molecules on human salivary gland cells. In this study we investigate a possible upregulation of FcgammaRs following anti-Ro and anti-La autoantibodies treatment. Anti-Ro and anti-La autoantibodies were purified from IgG fractions obtained from 14 patients with primary Sjögren's syndrome (SS), using Sepharose 4B-Ro and Sepharose 4B-La affinity columns. Flow cytometry and RT-PCR were used to study the FCgammaRI, FCgammaRII and FCgammaRIII receptors expression and upregulation by anti-Ro and anti-La on a salivary gland cell line. The present data document that the anti-Ro and anti-La autoantibodies determine an increase of the FcgammaRs expression on salivary gland cells, and provide evidence that both the high affinity FcgammaRI and the low affinity FcgammaRII and FcgammaRIII are overexpressed. Treatment with IgG isolated from healthy donors had no effect on the basal FCgammaRs expression.
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Registered trials
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