在接受Rituximab后HSCT后持续性低二球蛋白血症并不是由内在B细胞缺陷引起的
Lisa M Ott de Bruin1,2, Ingrid Pico-Knijnenburg1, Monique M van Ostaijen-Ten Dam1
1Laboratory for Pediatric Immunology, Willem-Alexander Children's Hospital, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
International journal of molecular sciences
|November 14, 2023
概括
在血造干细胞移植 (HSCT) 患者接受Rituximab (RTX) 治疗后,持久性低二球血症并不是由于内在B细胞缺陷或T辅助细胞减少. 这些患者的B细胞在体外仍能正常分化.
科学领域:
- 免疫学 免疫学 免疫学
- 血液学 血液学 血液学
- 移植医学 移植医学
背景情况:
- 利图西马布 (RTX) 用于造血干细胞移植 (HSCT) 治疗EBV相关的淋巴增殖性疾病和自身免疫性疾病,如自身免疫性血液溶解性贫血 (AIHA).
- 在RTX后,即使B细胞数量正常化后,也注意到持续的低血和依赖免疫球蛋白替代物的情况.
研究的目的:
- 为了调查在HSCT患者接受RTX治疗后持续的低血糖球蛋白血症是否是一种内在的B细胞缺陷.
主要方法:
- 分析了四名HSCT患者,在RTX后患有持续的低二球蛋白血症.
- 评估B细胞数量,记忆B细胞种群 (IgG+,IgA+),以及体外B细胞分化能力.
- 评估T细胞数量,包括CD4毛囊T辅助细胞 (Tfh).
主要成果:
- 患者的总B细胞数量正常,但缺乏或很低的IgG+记忆B细胞,通常是IgA+记忆B细胞.
- 试验室刺激表明,从这些患者中分类的天真B细胞可以分化为类切换记忆B细胞并产生IgA和IgG.
- 周围T细胞计数,包括Tfh细胞,在正常范围内.
结论:
- 在这些HSCT患者中,RTX后的持续性低二球蛋白血症并不是由内在B细胞缺陷引起的.
- 减少的Tfh细胞数量并不能解释观察到的低胺球蛋白血症.
- 该研究表明,在HSCT环境下,RTX后免疫球蛋白生产受损的可能是其他机制造成的.
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