Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at University of Gothenburg, and Rheumatology Clinic, Sahlgrenska University Hospital, Guldhedsgatan 10A, Gothenburg, 405 30, Sweden.
Arthritis Res Ther. 2010;12(3):R111. doi: 10.1186/ar3047. Epub 2010 Jun 8.
Rheumatoid arthritis (RA) is frequently complicated with infections. The aim of our study was to evaluate vaccination response in patients with RA after B-cell depletion by using rituximab.
Influenza (Afluria) and pneumococcal polysaccharides (Pneumo23) vaccines were given 6 months after rituximab (post-RTX group, n=11) or 6 days before rituximab treatment (pre-RTX group; n=8). RA patients never exposed to RTX composed the control group (n=10). Vaccine-specific cellular responses were evaluated on day 6 after vaccination, and vaccine-specific humoral responses, on day 21.
On day 6 after vaccination, formation of influenza-specific B cells was lower in post-RTX group as compared with the pre-RTX group and controls (P=0.04). Polysaccharide-specific B cells were found in 27% to 50%, being equally distributed between the groups. On day 21, the impairment of humoral responses was more pronounced with respect to influenza as compared with the pneumococcal vaccine and affected both IgG and light-chain production. Total absence of influenza-specific IgG production was observed in 55% of the post-RTX group.
RTX compromises cellular and humoral vaccine responses in RA patients. However, repeated RTX treatment or previous anti-tumor necrosis factor (anti-TNF) treatment did not accentuate these defects.
类风湿关节炎(RA)常伴有感染。我们的研究目的是评估利妥昔单抗(RTX)耗竭 B 细胞后 RA 患者的疫苗接种反应。
在利妥昔单抗(RTX)治疗后 6 个月(RTX 后组,n=11)或利妥昔单抗治疗前 6 天(RTX 前组;n=8)时给予流感(Afluria)和肺炎球菌多糖(Pneumo23)疫苗。从未接受过 RTX 治疗的 RA 患者为对照组(n=10)。在接种疫苗后第 6 天评估疫苗特异性细胞反应,在第 21 天评估疫苗特异性体液反应。
接种疫苗后第 6 天,RTX 后组流感特异性 B 细胞的形成低于 RTX 前组和对照组(P=0.04)。多糖特异性 B 细胞占 27%至 50%,在各组之间分布均匀。第 21 天,与肺炎球菌疫苗相比,流感疫苗的体液反应受损更为明显,影响 IgG 和轻链的产生。RTX 后组有 55%的患者完全缺乏流感特异性 IgG 产生。
RTX 会损害 RA 患者的细胞和体液疫苗反应。然而,重复的 RTX 治疗或先前的抗肿瘤坏死因子(anti-TNF)治疗并没有加重这些缺陷。