小柯机器人

美国犹他大学医学院June L. Round研究小组的发现，适应性免疫可引起共生真核生物之间的互利共生。相关论文于2021年7月14日在线发表在《自然》杂志上。

研究人员揭示了适应性免疫在促进真菌和宿主之间相互作用的功能。研究人员发现，潜在的致病性念珠菌物种会诱发肠道免疫球蛋白A（IgA）反应并成为其靶标。对白念珠菌的重点研究显示，专门用于粘附和入侵的致病性菌丝形态被肠道IgA反应优先锁定和抑制。小鼠和人类的IgA直接靶向局势富集的细胞表面粘附素。尽管通常是致病所需，但白念珠菌的菌丝不太适合在肠道定植，结果表明，针对菌丝的免疫选择提高了白念珠菌的竞争能力。白念珠菌会加剧肠道结肠炎，并且研究人员证明菌丝和一种IgA靶向的粘附素会加剧肠道损伤。

最后，研究人员使用临床相关的疫苗来诱导了粘附素特异性免疫反应，这可以保护小鼠在结肠炎期间免受白念珠菌相关的损害。这些研究结果表明，适应性免疫可以抑制有害的真菌效应分子，这对白念珠菌和其宿主都有好处。因此，IgA独特地解除了共生真菌的定植与致病机制之间的联系，进而促进稳态平衡。

据了解，致病性真菌居住在肠道微生物群中，但很少引起疾病。人们对真菌和免疫系统之间促进共生的相互作用知之甚少。

附：英文原文

Title: Adaptive immunity induces mutualism between commensal eukaryotes

Author: Kyla S. Ost, Teresa R. OMeara, W. Zac Stephens, Tyson Chiaro, Haoyang Zhou, Jourdan Penman, Rickesha Bell, Jason R. Catanzaro, Deguang Song, Shakti Singh, Daniel H. Call, Elizabeth Hwang-Wong, Kimberly E. Hanson, John F. Valentine, Kenneth A. Christensen, Ryan M. OConnell, Brendan Cormack, Ashraf S. Ibrahim, Noah W. Palm, Suzanne M. Noble, June L. Round

Issue&Volume: 2021-07-14

Abstract: Pathogenic fungi reside in the intestinal microbiota but rarely cause disease. Little is known about the interactions between fungi and the immune system that promote commensalism. Here we investigate the role of adaptive immunity in promoting mutual interactions between fungi and host. We find that potentially pathogenic Candida species induce and are targeted by intestinal immunoglobulin A (IgA) responses. Focused studies on Candida albicans reveal that the pathogenic hyphal morphotype, which is specialized for adhesion and invasion, is preferentially targeted and suppressed by intestinal IgA responses. IgA from mice and humans directly targets hyphal-enriched cell-surface adhesins. Although typically required for pathogenesis, C. albicans hyphae are less fit for gut colonization1,2 and we show that immune selection against hyphae improves the competitive fitness of C. albicans. C. albicans exacerbates intestinal colitis3 and we demonstrate that hyphae and an IgA-targeted adhesin exacerbate intestinal damage. Finally, using a clinically relevant vaccine to induce an adhesin-specific immune response protects mice from C. albicans-associated damage during colitis. Together, our findings show that adaptive immunity suppresses harmful fungal effectors, with benefits to both C. albicans and its host. Thus, IgA uniquely uncouples colonization from pathogenesis in commensal fungi to promote homeostasis.

DOI: 10.1038/s41586-021-03722-w

Source: https://www.nature.com/articles/s41586-021-03722-w

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