Mouse anti-Rat TCR alpha/beta Monoclonal antibody [clone S84], R-PE-Conjugated

2,5,6-Trichloro-1-(beta-D-ribofuranosyl)benzimidazole (TCRB) and certain analogues have shown significant activity against human cytomegalovirus. The metabolic instability of the glycosidic linkage in TCRB prompted us to synthesize the structurally similar imidazo[1,2-a]pyridine erythrofuranosyl C-nucleosides. As an approach to the synthesis of polychlorinated imidazo[1,2-alpyridine C-3-erythrofuranosides, a palladium-based methodology for coupling 2,3-dihydrofuran with chlorinated 3-iodoimidazo[1,2-a]pyridines was developed and optimized to give 80-90% yields of 2,6-dichloro- and 2,6,7-trichloro-3-(2,3-dideoxy-2,3-didehydro-D/L-erythrofuranosyl)imidazo[1,2-a]pyridine. Dihydroxylation of these didehydro derivatives with osmium tetroxide or with AD-mix alpha gave a mixture of erythrofuranosyl C-nucleosides that were separated by standard and then chiral chromatography. When screened for anti-HCMV and HSV-1 activity, the alpha-D anomer of 2,6,7-trichloro-3-(erythrofuranosyl)imidazo[1,2-alpyridine proved to be the most active member of the series, while the beta-anomers all proved to be inactive.

Objective. To evaluate the role of the T cell receptor beta chain locus (TCRB) in genetic susceptibility to rheumatoid arthritis (RA). Methods. Twenty-eight multiplex RA families were recruited from 3 rheumatology outpatient departments. All members were genotyped for a highly informative microsatellite (V(beta)6.7), a V(beta)12.2 SSCP marker, and a biallelic C-beta restriction fragment length polymorphism. Data were analyzed by the SIBPAL program to assess identity-by-descent in affected sib-pairs. Results. Using the V(beta)12.2 marker, there was suggestive evidence of increased sib-pair sharing (P = 0.005) in affected offspring (a P value of 0.001 is generally taken to establish linkage). Data for V(beta)6.7 and C-beta yielded significance levels of 0.06 and 0.19, respectively. Conclusion. These data suggest that a gene in or linked to the TCRB complex may confer genetic susceptibility to RA in these families. Confirmation in a larger panel of families is required.