多伦多大学Jennifer L. Gommerman小组的研究发现粘膜病毒感染通过1型滤泡辅助性T细胞引起长期的IgA反应。相关论文于2025年11月17日发表在《细胞》杂志上。
小组发现轮状病毒（RV）感染诱导肠道内的LLPCs产生高度突变的保护性IgA。与病毒特异性免疫球蛋白G (IgG)+ LLPCs不同，IgA+ LLPCs是独立于树突状细胞主要组织相容性复合体II类（MHC II类）的表达而产生的，相反，B细胞上的MHC II类是必要和充分的。B细胞-MHC II类也足以诱导T-bet+滤泡辅助性T （TFH1）细胞，这对于通过干扰素γ (IFNγ)和CXCR3依赖机制在肠道中积累RV特异性IgA+ LLPC至关重要。与RV感染类似，TFH1细胞是气道中流感特异性IgA反应所必需的。
然而，与RV感染不同的是，B细胞-MHC II类不足以诱导流感特异性IgA+ LLPCs，这表明存在粘膜部位特异性启动机制。总的来说，他们的数据显示，非常规启动的TFH1细胞支持IgA对粘膜病毒感染的反应。
据介绍，尽管免疫球蛋白A (IgA)+粘膜病毒感染后产生的长寿命浆细胞（LLPCs）提供持久的保护，防止再感染，但对它们的产生知之甚少。
附：英文原文
Title: Mucosal viral infection elicits long-lived IgA responses via type 1 follicular helper T cells
Author: Kei Haniuda, Natalie M. Edner, Yuko Makita, Sandhya Appiah, Tania H. Watts, Gregory F. Wu, Thamotharampillai Dileepan, Jennifer L. Gommerman
Issue&Volume: 2025-11-17
Abstract: Although immunoglobulin A (IgA)+ long-lived plasma cells (LLPCs) generated following mucosal viral infection provide durable protection against reinfection, little is known about their generation. Here, we show that rotavirus (RV) infection induces gut-resident LLPCs that produce highly mutated, protective IgA. Unlike RV-specific immunoglobulin G (IgG)+ LLPCs, IgA+ LLPCs were generated independently of major histocompatibility complex class II (MHC class II) expression by dendritic cells—rather, MHC class II on B cells was both necessary and sufficient. B cell-MHC class II was also sufficient to induce T-bet+ follicular helper T (TFH1) cells, which were crucial for RV-specific IgA+ LLPC accumulation in the gut via interferon γ (IFNγ)- and CXCR3-dependent mechanisms. Similar to RV infection, TFH1 cells were required for an influenza-specific IgA response in the airway. However, unlike RV infection, B cell-MHC class II was not sufficient to induce influenza-specific IgA+ LLPCs, suggesting the operation of mucosal-site-specific priming mechanisms. Collectively, our data reveal that unconventionally primed TFH1 cells support IgA responses to mucosal viral infections.
DOI: 10.1016/j.cell.2025.07.022
Source: https://www.cell.com/cell/abstract/S0092-8674(25)00812-8