One common effect of NF-kB over-activation in Rheumatoid arthritis, psoriasis & Crohn’s Disease
Key points:
- A receptor [A(3)AR] is associated with inflammation.
- It turns out that in rheumatoid arthritis, psoriasis and Crohn’s, there is ‘too much’ of this receptor on peripheral blood mononuclear cells (PBMCs) – a common thread.
- These same PBMCs also have ‘too much’ activated NF-kB – the ultimate common thread.
The publication:
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Cell Immunol. 2009;258(2):115-22. Epub 2009 May 7.
The anti-inflammatory target A(3) adenosine receptor is over-expressed in rheumatoid arthritis, psoriasis and Crohn’s disease.
Ochaion A, Bar-Yehuda S, Cohen S, Barer F, Patoka R, Amital H, Reitblat T, Reitblat A, Ophir J, Konfino I, Chowers Y, Ben-Horin S, Fishman P
Summary of the abstract
The Gi protein associated A(3) adenosine receptor (A(3)AR) was recently defined as a novel anti-inflammatory target.
The aim of this study was to look at A(3)AR expression levels in peripheral blood mononuclear cells (PBMCs) of patients with autoimmune inflammatory diseases and to explore transcription factors involved receptor expression.
Over-expression of A(3)AR was found in PBMCs derived from patients with rheumatoid arthritis (RA), psoriasis and Crohn’s disease compared with PBMCs from healthy subjects.
Bioinformatics analysis demonstrated the presence of DNA binding sites for nuclear factor-kappaB (NF-kappaB) and cyclic AMP-responsive element binding protein (CREB) in the A(3)AR gene promoter.
Up-regulation of NF-kappaB and CREB was found in the PBMCs from patients with RA, psoriasis and Crohn’s disease.
NF-kappaB and CREB are involved with the over-expression of A(3)AR in patients with autoimmune inflammatory diseases.
The receptor may be considered as a specific target to combat inflammation.
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