标题：RITUXIMAB AMELIORATES SKIN FIBROSIS THROUGH
REGULATING MYOFIBROBLASTIC ACTIVITY AND
TGE- B1 DIFFERENTIATION IN BLEOMYCIN-INDUCED
EXPERIMENTAL SCLERODERMA MODEL
摘要：Scleroderma (systemic sclerosis) is a chronic inflammatory disease that progresses with vascular damage, immunological abnormalities, and exten- sive fibrosis. Rituximab, an antibody against the B- lymphocyte-specific CD20 surface marker leads to depletion of B cell counts and functions. This study aims to investigate the protective efficacy of rituxi- mab on skin fibrosis in bleomycin (BLM) -induced experimental scleroderma model. This study in- cluded 4 groups of (n=7 for each group) Balb/c mice Group I mice were treated with subcutaneous 100 ul/day phosphate-buffered saline (PBS); while mice in Groups II, I1I, and IV were treated with subcuta- neous 100 μl/day BLM. Mice in Group IIl and Group IV were treated, intraperitoneally, with 50 ug and 250 ug rituximab, respectively; on the Ist and 14thdays ofthe experiment. Mice in all groups were sac- rificed at the end of the 4-week experimental period and tissue specimens were obtained. Serum levels of transforming growth factor (TGF)-B1, dermal thick-ness, the number of dermal inflammatory cells, andthe number of a smooth muscle actin positive cells (a-SMA+) were determined. The administration of BLM increased the inflammatory cell infiltration of the dermis, a-SMA+ cell counts in the dermis, and dermal thickness. However, rituximab treatments decreased inflammatory cell infiltrations, a-SMA+ cell counts and dermal thickness, in the BLM in- jected mice. Both rituximab doses had similar anti- fibrotic efficacy. Rituximab prevents the develop- ment of fibrosis in a BLM-induced experimental scleroderma model. This result suggests that rituxi-mab may be a effective therapeutic agent in patients with early-stage scleroderma.
