Charité Universitätsmedizin Berlin and Deutsches Rheumaforschungszentrum, Berlin, Germany.
Charité Universitätsmedizin Berlin and Deutsches Rheumaforschungszentrum, Berlin, Germany, and Universidad de Antioquia, Medellín, Colombia.
Arthritis Rheumatol. 2022 Jun;74(6):934-947. doi: 10.1002/art.42060. Epub 2022 Apr 17.
Patients with autoimmune inflammatory rheumatic diseases receiving rituximab (RTX) therapy are at higher risk of poor COVID-19 outcomes and show substantially impaired humoral immune response to anti-SARS-CoV-2 vaccine. However, the complex relationship between antigen-specific B cells and T cells and the level of B cell repopulation necessary to achieve anti-vaccine responses remain largely unknown.
Antibody responses to SARS-CoV-2 vaccines and induction of antigen-specific B and CD4/CD8 T cell subsets were studied in 19 patients with rheumatoid arthritis (RA) or antineutrophil cytoplasmic antibody-associated vasculitis receiving RTX, 12 patients with RA receiving other therapies, and 30 healthy controls after SARS-CoV-2 vaccination with either messenger RNA or vector-based vaccines.
A minimum of 10 B cells per microliter (0.4% of lymphocytes) in the peripheral circulation appeared to be required for RTX-treated patients to mount seroconversion to anti-S1 IgG upon SARS-CoV-2 vaccination. RTX-treated patients who lacked IgG seroconversion showed reduced receptor-binding domain-positive B cells (P = 0.0005), a lower frequency of Tfh-like cells (P = 0.0481), as well as fewer activated CD4 (P = 0.0036) and CD8 T cells (P = 0.0308) compared to RTX-treated patients who achieved IgG seroconversion. Functionally relevant B cell depletion resulted in impaired interferon-γ secretion by spike-specific CD4 T cells (P = 0.0112, r = 0.5342). In contrast, antigen-specific CD8 T cells were reduced in both RA patients and RTX-treated patients, independently of IgG formation.
In RTX-treated patients, a minimum of 10 B cells per microliter in the peripheral circulation is a candidate biomarker for a high likelihood of an appropriate cellular and humoral response after SARS-CoV-2 vaccination. Mechanistically, the data emphasize the crucial role of costimulatory B cell functions for the proper induction of CD4 responses propagating vaccine-specific B cell and plasma cell differentiation.
接受利妥昔单抗(RTX)治疗的自身免疫性炎症性风湿病患者发生 COVID-19 不良结局的风险较高,并且对 SARS-CoV-2 疫苗的体液免疫反应明显受损。然而,抗原特异性 B 细胞与 T 细胞之间的复杂关系以及实现疫苗反应所需的 B 细胞再增殖水平在很大程度上仍不清楚。
研究了 19 例接受 RTX 治疗的类风湿关节炎(RA)或抗中性粒细胞胞质抗体相关性血管炎患者、12 例接受其他治疗的 RA 患者和 30 例健康对照者在接种 SARS-CoV-2 信使 RNA 或基于载体疫苗后的 SARS-CoV-2 疫苗抗体反应和抗原特异性 B 细胞和 CD4/CD8 T 细胞亚群的诱导。
接受 RTX 治疗的患者在接种 SARS-CoV-2 疫苗后要产生针对 S1 IgG 的血清转化,似乎需要外周血循环中每微升至少 10 个 B 细胞(占淋巴细胞的 0.4%)。未发生 IgG 血清转化的 RTX 治疗患者表现出结合域阳性 B 细胞减少(P = 0.0005)、滤泡辅助样 T 细胞频率降低(P = 0.0481)、以及激活的 CD4(P = 0.0036)和 CD8 T 细胞减少(P = 0.0308),与发生 IgG 血清转化的 RTX 治疗患者相比。功能相关的 B 细胞耗竭导致 Spike 特异性 CD4 T 细胞干扰素-γ分泌受损(P = 0.0112,r = 0.5342)。相反,抗原特异性 CD8 T 细胞在 RA 患者和接受 RTX 治疗的患者中均减少,而与 IgG 形成无关。
在接受 RTX 治疗的患者中,外周血循环中每微升至少 10 个 B 细胞是 SARS-CoV-2 疫苗接种后细胞和体液反应可能性高的候选生物标志物。从机制上讲,这些数据强调了共刺激 B 细胞功能对于适当诱导 CD4 反应从而促进疫苗特异性 B 细胞和浆细胞分化的关键作用。