Our objective was to evaluate the immunogenicity of branded and biosimilar infliximab\nby detecting changes in T-helper-9 (Th9) percentages induced by an in vitro stimulation test.\nMethods: Peripheral blood mononuclear cells collected from 55 consecutive rheumatoid arthritis\n(RA) outpatients (15 drug free, 20 successfully treated with branded infliximab, 20 branded\ninfliximab inadequate responders) and 10 healthy controls were cultured, with or without 50 Ã?¼g/mL\nof infliximab originator (RemicadeÃ?®) or 50 Ã?¼g/mL of infliximab biosimilar (RemsimaÃ?®) for 18 h.\nTh9 lymphocytes were identified by means of flow cytometry as PU.1 and IRF4-expressing,\nIL-9-secreting CD4+ T cells. Furthermore, the markers CCR7 and CD45RA were used to\ndistinguish naÃ?¯ve from memory IL-9 producer cells. Results: Under unstimulated conditions,\nthe drug-free RA patients had the highest percentages of Th9 lymphocytes. Following stimulation\nwith branded infliximab, the percentages of PU.1 and IRF4-expressing Th9 cells, CCR7+, CD45RAâË?â??\n(central memory) and CCR7âË?â??, CD45RAâË?â?? (effector memory) cells significantly increased in the group\nof inadequate responders, but no significant variation was observed after exposure to the biosimilar\nof infliximab. Conclusions: Th9 cells seem to be involved in the immune response to the epitopes of\nbranded, but not biosimilar, infliximab, and this may depend on the recall and stimulation of both\ncentral and effector memory cells.
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