Anti-CD45 monoclonal antibody, clone YW62.3 [Biotin]

Rheumatoid arthritis (RA) is a chronic inflammatory disease that affects "1% of the Caucasian population. Over the last decades, the availability of biological drugs targeting the proinflammatory cytokine tumour necrosis factor a, anti-TNF drugs, has improved the treatment of patients with RA. However, one-third of the patients do not respond to the treatment. We wanted to evaluate the status of pharmacogenomics of anti-TNF treatment. We performed a PubMed literature search and all studies reporting original data on associations between genetic variants and anti-TNF treatment response in RA patients were included and results evaluated by meta-analysis. In total, 25 single nucleotide polymorphisms were found to be associated with anti-TNF treatment response in RA (19 from genome-wide association studies and 6 from the meta-analyses), and these map to genes involved in T cell function, NFKB and TNF signalling pathways (including CTCN5, TEC, PTPRC, FCGR2A, NFKBIB, FCGR2A, IRAK3). Explorative prediction analyses found that biomarkers for clinical treatment selection are not yet available.

In this study, we investigate the role of the C --> G mutation in position 77 of exon 4 of the protein tyrosine phosphatase receptor-type C (PTPRC) gene, coding for the CD45 molecule, for the development of multiple sclerosis (MS) in an Italian continental population. The PTPRC mutated genotype has been recently described as associated with MS in three different case-control studies carried out in German MS patients, whereas similar studies performed in the US and Swedish populations failed to demonstrate such an association. The C --> G transition in position 77 was found in a small number of Italian MS patients and in none of the matched group of healthy controls (Fisher exact test, P value = 0.02). This finding suggests a role, in at least a group of patients, for the PTPRC mutation in genetic susceptibility to MS. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.