International immunology最新文献_第5页

Repeated mRNA vaccination and breakthrough infection reveal durable dominance but diminishing recall of vaccine-induced CD8⁺ T-cell clones. 重复的mRNA接种和突破性感染显示出持久的优势，但疫苗诱导的CD8 + t细胞克隆的召回率逐渐降低。

IF 3.4 4区医学

International immunology Pub Date : 2026-06-01 DOI: 10.1093/intimm/dxag004

Peng Xu, Satoshi Ueha, Hiroyasu Aoki, Masahiro Kitabatake, Mingyu Chen, Shigeyuki Shichino, Atsushi Hara, Noriko Ouji-Sageshima, Toshihiro Ito, Chihiro Motozono, Kouji Matsushima

{"title":"Repeated mRNA vaccination and breakthrough infection reveal durable dominance but diminishing recall of vaccine-induced CD8⁺ T-cell clones.","authors":"Peng Xu, Satoshi Ueha, Hiroyasu Aoki, Masahiro Kitabatake, Mingyu Chen, Shigeyuki Shichino, Atsushi Hara, Noriko Ouji-Sageshima, Toshihiro Ito, Chihiro Motozono, Kouji Matsushima","doi":"10.1093/intimm/dxag004","DOIUrl":"10.1093/intimm/dxag004","url":null,"abstract":"Successive mRNA vaccinations preserve severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-specific T-cell immunity, but how individual CD8⁺ T-cell clones behave across repeated booster doses and breakthrough infection (BTI) remains poorly defined. We longitudinally tracked bulk CD8⁺ T-cell receptor beta (TCRβ) repertoires and spike-specific tetramer⁺ CD8⁺ T cells in adult participants across the third and fourth vaccine doses and subsequent BTI. Each booster continued to recruit previously unexpanded \"new\" responder clonotypes, but both the number and summed frequency of newly engaged clones declined with successive doses. In contrast, clones first recruited by the initial prime-boost doses-particularly those expanded after Dose 2-formed a durable, hierarchically dominant memory pool that persisted for >2 years yet displayed progressively attenuated recall with later boosters. BTI revealed a complementary mode of repertoire remodeling: newly engaged clones that had not responded to prior vaccinations showed the strongest, but transient, expansion, broadening the antigenic targets beyond spike. On the other hand, vaccine-induced clones showed limited recall response while sustaining their dominance in the long term. Together, these findings indicate that repeated mRNA vaccination maintains a stable pool of early-established CD8⁺ T-cell clones but progressively limits their recall capacity, whereas BTI mobilizes additional, partially distinct clonotypes that expand robustly and broaden antigenic coverage.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"371-382"},"PeriodicalIF":3.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145989166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

T-cell help is a limiting factor for rare anti-influenza memory B cells to re-enter germinal centers and generate potent broadly neutralizing antibodies. T细胞帮助是罕见的抗流感记忆B细胞重新进入生发中心并产生有效的广泛中和抗体的限制因素。

IF 3.4 4区医学

International immunology Pub Date : 2026-06-01 DOI: 10.1093/intimm/dxag003

Yang Xue, Yuki Tai, Hiromi Yamamoto, Daiki Mori, Kaori Sakai, Takuya Miyazaki, Mikito Owa, Kohei Kometani, Isao Ebina, Ryusuke Omiya, Kunihiro Hattori, Takeshi Inoue, Wataru Ise, Ryo Shinnakasu, Tomohiro Kurosaki

{"title":"T-cell help is a limiting factor for rare anti-influenza memory B cells to re-enter germinal centers and generate potent broadly neutralizing antibodies.","authors":"Yang Xue, Yuki Tai, Hiromi Yamamoto, Daiki Mori, Kaori Sakai, Takuya Miyazaki, Mikito Owa, Kohei Kometani, Isao Ebina, Ryusuke Omiya, Kunihiro Hattori, Takeshi Inoue, Wataru Ise, Ryo Shinnakasu, Tomohiro Kurosaki","doi":"10.1093/intimm/dxag003","DOIUrl":"10.1093/intimm/dxag003","url":null,"abstract":"The development of vaccines eliciting broadly neutralizing influenza antibodies (bnAbs) is an extraordinary challenge. One hypothetical proposal is that CD4+ T-cell help to rare immuno-subdominant bnAb class memory B cells is one critical factor to cause these B cells to re-enter secondary germinal centers (GCs) and generate potent bnAbs. In this regard, we previously showed that the prototypic hemagglutinin stem vaccine does not contain the dominant CD4+ T-cell epitope. Here, to test the above hypothesis, we examined the effects of adding a single influenza T-cell epitope to the stem vaccine in an influenza pre-infected booster mouse model. We found that this fused booster vaccine efficiently recruited antistem memory B cells with prior GC experience into the secondary GCs in draining lymph nodes. Furthermore, these secondary GC-experienced cells evolved, thereby contributing to generation of more potent neutralizing activity toward variant viruses. Thus, our results suggest the importance of T-cell help in generating potent bnAbs by recruiting rare subdominant memory B cells into secondary GCs, and have implications for vaccine design.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"383-395"},"PeriodicalIF":3.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145989171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Epitope specificity shapes the CD4+ T-cell response to influenza virus infection in mice. 表位特异性决定了小鼠对流感病毒感染的CD4+ T细胞反应。

IF 3.4 4区医学

International immunology Pub Date : 2026-06-01 DOI: 10.1093/intimm/dxag008

Daiki Mori, Nicolas Sax, Nozomi Shimada, Mana Kuwabara, Isao Ebina, Ryusuke Omiya, Kunihiro Hattori, Ryo Shinnakasu, Kazuo Yamashita, Sho Yamasaki, Tomohiro Kurosaki, Wataru Ise

{"title":"Epitope specificity shapes the CD4+ T-cell response to influenza virus infection in mice.","authors":"Daiki Mori, Nicolas Sax, Nozomi Shimada, Mana Kuwabara, Isao Ebina, Ryusuke Omiya, Kunihiro Hattori, Ryo Shinnakasu, Kazuo Yamashita, Sho Yamasaki, Tomohiro Kurosaki, Wataru Ise","doi":"10.1093/intimm/dxag008","DOIUrl":"10.1093/intimm/dxag008","url":null,"abstract":"CD4+ T helper (Th) cells play a central role in orchestrating protective immune responses during infection and vaccination. Activation of naïve CD4+ T cells is initiated by the recognition of antigenic peptides presented on MHC class II (MHC-II) molecules, leading to their differentiation into distinct effector subsets. In the context of influenza virus infection, the quality of CD4+ T-cell responses is a critical determinant of both cellular and humoral immunity. Given the limited breadth of protection conferred by current influenza vaccines, which primarily induce strain-specific neutralizing antibodies, there is growing interest in harnessing CD4+ T-cell responses targeting conserved viral epitopes to achieve broader and more durable protection. Identifying potent T-cell epitopes within viral antigens is therefore critical for designing effective vaccines that elicit robust, durable, and cross-protective Th-cell and antibody responses. In this study, using a mouse model of influenza virus infection, we identified CD4+ T-cell epitopes within the hemagglutinin (HA) and nucleoprotein (NP) of the H1N1 strain. We generated two NP peptide/MHC-II tetramers, NP264-274/I-Ab and NP418-428/I-Ab, which enabled in vivo tracking and characterization of epitope-specific CD4+ T cells during infection. These epitope-specific T cells exhibited distinct T-cell receptor (TCR) repertoires and differentiation patterns toward either Th1 or T follicular helper (Tfh) lineages, suggesting that epitope specificity shapes the quality of the T-cell response. Our findings provide new insights into the epitope-dependent functional diversity of Th-cell responses and offer valuable tools for the rational design of broadly protective influenza vaccines.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"396-405"},"PeriodicalIF":3.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Salmonella Typhimurium evades from host immunity and antibiotics in monocytes. 鼠伤寒沙门氏菌在单核细胞中逃避宿主免疫和抗生素。

IF 3.4 4区医学

International immunology Pub Date : 2026-05-07 DOI: 10.1093/intimm/dxaf077

Uki Kimura, Nobuhiro Matsuyama, Karen Saiki, Sei Kashima, Hiroki Takahashi, Akiko Takaya, Koji Tokoyoda

引用次数: 0

Zika virus exacerbates encephalomyelitis by inducing the production of T cell-attracting chemokines in astrocytes. 寨卡病毒通过诱导星形胶质细胞产生吸引T细胞的趋化因子而加剧EAE。

IF 3.4 4区医学

International immunology Pub Date : 2026-05-07 DOI: 10.1093/intimm/dxaf075

Naganori Kamiyama, Benjawan Saechue, Nozomi Sachi, Thanyakorn Chalalai, Astri Dewayani, Masaaki Okamoto, Sotaro Ozaka, Yasuhiro Soga, Yomei Kagoshima, Supanuch Ekronarongchai, Shinya Hidano, Makoto Tsuda, Takashi Kobayashi

{"title":"Zika virus exacerbates encephalomyelitis by inducing the production of T cell-attracting chemokines in astrocytes.","authors":"Naganori Kamiyama, Benjawan Saechue, Nozomi Sachi, Thanyakorn Chalalai, Astri Dewayani, Masaaki Okamoto, Sotaro Ozaka, Yasuhiro Soga, Yomei Kagoshima, Supanuch Ekronarongchai, Shinya Hidano, Makoto Tsuda, Takashi Kobayashi","doi":"10.1093/intimm/dxaf075","DOIUrl":"10.1093/intimm/dxaf075","url":null,"abstract":"Recent outbreaks of the ZIKA virus (ZIKV) in Brazil and Puerto Rico have been linked to an increase in the incidence of fetal microcephaly and Guillain-Barré syndrome. In addition, although a causal relationship remains unproven, ZIKV has been found in the brains of multiple sclerosis (MS) patients, prompting interest in a possible link. The present study aimed to elucidate the role of ZIKV in the pathogenesis of MS. ZIKV-infected mice with experimental autoimmune encephalomyelitis (EAE) exhibited aggravated EAE symptoms with significant demyelination of the central nervous system (CNS). Moreover, ZIKV infection promoted pathogenic T cell infiltration into the CNS by enhancing the expression of chemokines for C-C motif chemokine receptor 2 (CCR2) in astrocytes, which was dependent on tumor necrosis factor receptor-associated factor 6 (TRAF6) signaling. Propagermanium, a CCR2 inhibitor, prevented ZIKV-induced exacerbation of EAE in mice. These findings highlight the critical role of TRAF6 signaling in the progression of neurological disorders caused by ZIKV infection.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"318-334"},"PeriodicalIF":3.4,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13150445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145767896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TLR7 responses to nucleosides drive sialadenitis in Slc29a3-deficient mice. TLR7对核苷的反应驱动slc29a3缺陷小鼠的涎腺炎。

IF 3.4 4区医学

International immunology Pub Date : 2026-05-07 DOI: 10.1093/intimm/dxaf073

Takuma Shibata, Kotono Okabe-Kibe, Hu Chen, Kiyoshi Yamaguchi, Daisuke Koga, Masato Taoka, Yuji Motoi, Ryota Sato, Hao-Wen Hsiao, Ryutaro Fukui, Naoki Kaneko, Zhiqin Wang, Yanmei Li, Wei Wei, Zhigang Cai, Yoichi Furukawa, Emi K Nishimura, Shintaro Kawano, Masafumi Moriyama, Seiji Nakamura, Kensuke Miyake

{"title":"TLR7 responses to nucleosides drive sialadenitis in Slc29a3-deficient mice.","authors":"Takuma Shibata, Kotono Okabe-Kibe, Hu Chen, Kiyoshi Yamaguchi, Daisuke Koga, Masato Taoka, Yuji Motoi, Ryota Sato, Hao-Wen Hsiao, Ryutaro Fukui, Naoki Kaneko, Zhiqin Wang, Yanmei Li, Wei Wei, Zhigang Cai, Yoichi Furukawa, Emi K Nishimura, Shintaro Kawano, Masafumi Moriyama, Seiji Nakamura, Kensuke Miyake","doi":"10.1093/intimm/dxaf073","DOIUrl":"10.1093/intimm/dxaf073","url":null,"abstract":"Autoimmune sialadenitis is a hallmark of IgG4-related disease (IgG4-RD) and Sjögren syndrome. The single-stranded RNA sensor TLR7 has been shown as a driver of sialadenitis. Although TLR7 is activated by ssRNA degradation products such as nucleosides and oligoribonucleotides, the role of these ligands in sialadenitis development remains unclear. Here, we demonstrate that lysosomal accumulation of endogenous nucleosides is sufficient to drive autoimmune sialadenitis. Loss-of-function genetic variations in the nucleoside transporter SLC29A3 cause lysosomal nucleoside accumulation, leading to constitutive activation of TLR7 and TLR8 in monocytes and macrophages. Consequently, macrophages infiltrate multiple organs in mice and humans. In Slc29a3-/- mice, submandibular glands (SMGs) were impaired in saliva production. SLC29A3-deficiency specifically damaged Aqp5+ acinar and intercalated duct cells in SMGs, while sparing neighboring cells such as ductal and myoepithelial cells. Although macrophages accumulated in both the spleen and SMGs, lymphocyte infiltration and production of chemokines, including CXCL9, CXCL13, and CCL5, occurred selectively in SMGs. In IgG4-RD patients, these chemokines were also produced in SMGs, highlighting parallels between sialadenitis in Slc29a3-/- mice and IgG4-RD. These findings indicate that constitutive TLR7 activation by nucleosides is a key mechanism driving autoimmune sialadenitis.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"306-317"},"PeriodicalIF":3.4,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145661058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Generation of CD68+ macrophage-depleted NOG mice for in vivo engraftment of human red blood cells. CD68+巨噬细胞耗尽NOG小鼠体内植入人红细胞的实验研究。

IF 3.4 4区医学

International immunology Pub Date : 2026-05-07 DOI: 10.1093/intimm/dxaf072

Yusuke Ohno, Misa Mochizuki, Kenji Kawai, Motohito Goto, Riichi Takahashi, Ryoji Ito

{"title":"Generation of CD68+ macrophage-depleted NOG mice for in vivo engraftment of human red blood cells.","authors":"Yusuke Ohno, Misa Mochizuki, Kenji Kawai, Motohito Goto, Riichi Takahashi, Ryoji Ito","doi":"10.1093/intimm/dxaf072","DOIUrl":"10.1093/intimm/dxaf072","url":null,"abstract":"Humanized mice are invaluable models for investigating human cell engraftment in vivo post-transplantation. Mice engrafted with human red blood cells (hRBCs) are useful for examining the physiological roles of hRBCs in vivo, including studies on blood disorders, immune responses, and transfusion-related research. These models hold promise for malaria infection studies and vaccine development. However, engrafted hRBCs in vivo in immunodeficient mice present challenges that must be addressed to establish effective in vivo models. In this study, we explored the rejection mechanisms of hRBCs in immunodeficient NOD/Shi-scid-IL2rγnull (NOG) mice and developed a novel model for long-term RBC engraftment. We observed rapid depletion of fluorescently labeled hRBCs in the liver, but not in other organs, of NOG mice, with Gr-1midCD68+ mouse macrophages playing a significant role in the elimination of hRBCs in the liver. To counteract this, we created thymidine kinase (TK) transgenic (Tg) mice under the human CD68 promoter (NOG-pCD68-TK Tg), which, upon administration of valganciclovir (VGCV), led to the successful depletion of macrophages. Consequently, hRBCs showed significantly prolonged engraftment in NOG-pCD68-TK Tg mice compared to non-Tg mice following macrophage depletion, maintaining engraftment for up to 14 d post-transplantation. This study elucidates the erythrophagocytosis mechanisms of hRBCs in mice and establishes NOG-pCD68-TK Tg mice as a valuable model for the long-term engraftment of hRBCs, potentially advancing in vivo hRBC research.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"296-305"},"PeriodicalIF":3.4,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145661039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Microbiota regulation of gut-brain neuroimmune crosstalk in early life. 生命早期肠道-脑神经免疫串扰的微生物群调节。

IF 3.4 4区医学

International immunology Pub Date : 2026-05-07 DOI: 10.1093/intimm/dxaf076

Purnima Ravisankar, Daniel S H Wong, Melody Y Zeng

引用次数: 0

Repetitive fasting-refeeding enhances metformin-induced CXCR6+ CD8+ T cell tumor infiltration via VCAM-1 upregulation on normalized vasculature during refeeding. 重复禁食-再摄食通过再摄食期间VCAM-1上调对正常脉管系统的影响增强二甲双胍诱导的CXCR6+ CD8+T细胞肿瘤浸润

IF 3.4 4区医学

International immunology Pub Date : 2026-04-01 DOI: 10.1093/intimm/dxaf068

Weiyang Zhao, Miho Tokumasu, Mikako Nishida, Natsumi Imano, Nahoko Yamashita, Heiichiro Udono

{"title":"Repetitive fasting-refeeding enhances metformin-induced CXCR6+ CD8+ T cell tumor infiltration via VCAM-1 upregulation on normalized vasculature during refeeding.","authors":"Weiyang Zhao, Miho Tokumasu, Mikako Nishida, Natsumi Imano, Nahoko Yamashita, Heiichiro Udono","doi":"10.1093/intimm/dxaf068","DOIUrl":"10.1093/intimm/dxaf068","url":null,"abstract":"Fasting is known to alter the circulation dynamics of immune cells, including T cells, by shifting them from peripheral tissues to the bone marrow (BM), where they enter a quiescent state to avoid starvation stress and acquire apoptosis resistance through upregulation of BCL2. Upon refeeding, these T cells exit the BM and return to circulation. In solid tumors, fasting-refeeding not only affects the trafficking of CD8+ T cells between tumors and their draining lymph nodes (dLNs); but also modulates the antitumor immune response. In this study, we investigated how metformin's antitumor responses are affected by repeated fasting-refeeding cycles. Metformin administration combined with weekly 48-hour fasting showed a synergistic antitumor effect, which was abolished by in vivo depletion of CD8+ T cells. Immunohistofluorescence staining showed that fasting reduced CD8+ T cells in tumors and dLNs while increasing their presence in the BM; refeeding reversed this distribution. Refeeding also increased the expression of Ifng, Gzmb, Tnf, and Tbx21 in tumors. Likewise, Cxcr6, Cxcl16, and Vcam1 expression levels were elevated only upon refeeding. Notably, CXCR6 was exclusively expressed on CD62L- effector memory T cells (TEM). The antitumor effect induced by the combinational therapy was abolished by administration of an anti-VCAM-1 neutralizing antibody. Our findings demonstrate that combining metformin with fasting exerts a synergistic antitumor effect by recruiting CD8+ T cells-relocated to the BM during fasting-back to the tumor during refeeding, facilitated by enhanced VCAM-1 expression on normalized tumor vasculature.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"251-263"},"PeriodicalIF":3.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145495394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Microniche control of innate lymphocyte biology in the gut. 肠道先天淋巴细胞生物学的微显微控制。

IF 3.4 4区医学

International immunology Pub Date : 2026-04-01 DOI: 10.1093/intimm/dxaf071

Brooke E Towers, Gregory F Sonnenberg

{"title":"Microniche control of innate lymphocyte biology in the gut.","authors":"Brooke E Towers, Gregory F Sonnenberg","doi":"10.1093/intimm/dxaf071","DOIUrl":"10.1093/intimm/dxaf071","url":null,"abstract":"The human gastrointestinal tract is a unique mucosal barrier with a tremendous surface area that is subject to continuous exposure to the environment. The immune system must remain poised to protect this organ system from potential pathogens while restraining chronic inflammatory responses that negatively impact physiological functions or facilitate malignancy. Innate lymphocytes emerged as major regulators of gut health through numerous key functions. Recent evidence indicates that these cells are adaptively influenced by specialized microniches, or distinct aggregates of cells that engage in dynamic crosstalk at a microscopic level and integrate signals from the environment to perform specialized functions with regional precision. Here, we explore our current understanding of how microniches in the gut shape the biology of innate lymphocytes, with a focus on an interplay of diet and microbial exposure, selective cell-cell communication networks, and spatiotemporal properties. We also discuss how these microniches may be altered in human diseases or could be harnessed to better protect the gut. Finally, we identify current gaps in knowledge in this rapidly emerging field.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"222-235"},"PeriodicalIF":3.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13042245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145540428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0