International immunology最新文献

Role of group 2 innate lymphoid cells in intranasal sensitization-induced allergic rhinitis in mice. 2组先天淋巴样细胞在小鼠鼻内致敏性变应性鼻炎中的作用。

IF 3.2 4区医学

International immunology Pub Date : 2025-10-08 DOI: 10.1093/intimm/dxaf060

Yukinori Kato, Tetsuji Takabayashi, Anna Shimizu, Ayako Maegawa, Eiichi Kato, Naoto Adachi, Keisuke Koyama, Kyoko Saito, Kanako Yoshida, Masanori Kidoguchi, Taiyo Morikawa, Yoshimasa Imoto, Masafumi Sakashita, Mamoru Ito, Masato Kubo, Shigeharu Fujieda

{"title":"Role of group 2 innate lymphoid cells in intranasal sensitization-induced allergic rhinitis in mice.","authors":"Yukinori Kato, Tetsuji Takabayashi, Anna Shimizu, Ayako Maegawa, Eiichi Kato, Naoto Adachi, Keisuke Koyama, Kyoko Saito, Kanako Yoshida, Masanori Kidoguchi, Taiyo Morikawa, Yoshimasa Imoto, Masafumi Sakashita, Mamoru Ito, Masato Kubo, Shigeharu Fujieda","doi":"10.1093/intimm/dxaf060","DOIUrl":"https://doi.org/10.1093/intimm/dxaf060","url":null,"abstract":"Cells of the innate immune system, specifically group 2 innate lymphoid cells (ILC2s), play an important role in type 2 inflammation. However, their involvement in allergic rhinitis remains unclear. Thus, in this study, we aimed to clarify the role of ILC2s and acquired immune responses in the onset of allergic rhinitis induced via intranasal mucosal sensitization with antigens in mice. Naive mice were intranasally administered antigens for short-term (4 consecutive days) or long-term (21 consecutive days). The number of sneezes, serum-specific immunoglobulin E (IgE) levels, and eosinophil infiltration in the nasal mucosa were subsequently assessed. Short-term intranasal antigen administration to naive mice induced eosinophilic inflammation of the nasal mucosa in an acquired immune-independent and protease- and ILC2-dependent manner. Antigen-independent sneezing was caused by a calcium influx response via transient receptor potential vanilloid channels. By contrast, long-term intranasal mucosal sensitization with antigens led to the onset of allergic rhinitis. Furthermore, increased serum-specific IgE levels and sneezing frequency, as well as significant eosinophilic infiltration, were observed in the nasal mucosa. ILC2s in the nasal mucosa did not proliferate upon short-term stimulation with antigens but proliferated upon long-term stimulation, facilitating acquired immunity and allergic rhinitis onset. Our findings demonstrated that allergic inflammation is induced by the protease/IL-33/ILC2/IL-5 axis during the initiator phase. Acquired immunity induced by long-term sensitization and innate immunity facilitated by short-term sensitization together induce significant allergic inflammation and allergic rhinitis onset.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145250950","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

Functional Diversity and Tissue-Specific Regulation of Group 2 Innate Lymphoid Cells in Barrier Immunity. 第2组先天淋巴样细胞在屏障免疫中的功能多样性和组织特异性调控。

IF 3.2 4区医学

International immunology Pub Date : 2025-10-08 DOI: 10.1093/intimm/dxaf062

Mitsuki Ito, Yunzi Yan, Naoko Satoh-Takayama

{"title":"Functional Diversity and Tissue-Specific Regulation of Group 2 Innate Lymphoid Cells in Barrier Immunity.","authors":"Mitsuki Ito, Yunzi Yan, Naoko Satoh-Takayama","doi":"10.1093/intimm/dxaf062","DOIUrl":"https://doi.org/10.1093/intimm/dxaf062","url":null,"abstract":"Group 2 innate lymphoid cells (ILC2s) contribute to the maintenance of tissue homeostasis by promoting tissue repair and regulating immune responses. However, excessive or prolonged activation of ILC2s can induce chronic inflammation and tissue fibrosis, thereby contributing to disease exacerbation and progression. Recent studies have revealed that the mechanisms underlying ILC2 activation and their effector functions vary considerably across different tissues. Therefore, understanding the tissue-specific regulation and function of ILC2s is essential for elucidating their roles in both physiological and pathological contexts. Here, we highlight the distinct functional roles of ILC2s in the stomach, intestine, lung, and skin. We examine the differences in activation cues and key effector cytokines produced by ILC2s, illustrating how these cells adapt to the unique immune environments of each tissue. Furthermore, although ILC2s were once thought to function independently of the microbiota, recent findings suggest that microbial communities may influence their activation and function. We also discuss the emerging roles of ILC2s in various diseases, including allergies, inflammatory disorders, and cancer, emphasizing their dual roles in both host defense and disease exacerbation. Gaining a deeper understanding of the distinct functional roles of ILC2s across different tissues will enhance our insight into their involvement in disease pathogenesis and may open new avenues for targeted therapeutic strategies that modulate ILC2 responses.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145250939","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

Interaction between neurons and microglia in healthy and disease states. 健康和疾病状态下神经元和小胶质细胞之间的相互作用。

IF 3.2 4区医学

International immunology Pub Date : 2025-09-26 DOI: 10.1093/intimm/dxaf057

Ayaka Nakamura, Takashi Shichita

{"title":"Interaction between neurons and microglia in healthy and disease states.","authors":"Ayaka Nakamura, Takashi Shichita","doi":"10.1093/intimm/dxaf057","DOIUrl":"https://doi.org/10.1093/intimm/dxaf057","url":null,"abstract":"Interactions between neurons and microglia are essential for various brain functions under both healthy and pathological states. Microglia have classical functions as immune cells, causing cerebral inflammation, whereas their reparative roles after acute cerebral inflammation have recently attracted attention. In the healthy brain state, microglia contribute to homeostasis and brain tissue development. Microglia regulate neuronal activity by responding to molecules derived from neurons and eliminating excess synapses to achieve normal brain development and maintain a homeostatic brain environment. Microglia are also involved in neuronal information processing, such as learning and memory, by modulating synaptic remodeling and neurogenesis. In contrast, aging alters brain homeostasis and increases vulnerability to neurodegenerative pathologies through changes in interactions between neurons and microglia. Microglia exert diverse functions in neurological and psychiatric diseases. Microglia are responsible for rapid inflammatory responses by receiving abnormal signals from injured brain cells. Excess neuroinflammation mediated by disease-associated microglia exacerbates the pathology of central nervous system (CNS) diseases. Recent studies have also revealed the roles of microglia in improving pathologies through the phagocytosis of neurotoxic proteins and damaged or excess synapses. This review highlights the interaction between neurons and microglia in both healthy and pathological brain states. Understanding these interactions could lead to the development of therapeutic strategies by regulating the pathologies underlying various CNS disorders.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148971","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

Neuroprotective crosstalk from vitamin B12 and sphingolipid signaling pathways in therapy for multiple sclerosis. 来自维生素B12和鞘脂信号通路的神经保护串扰在多发性硬化治疗中的作用。

IF 3.2 4区医学

International immunology Pub Date : 2025-09-25 DOI: 10.1093/intimm/dxaf058

Yasuyuki Kihara, Jerold Chun

{"title":"Neuroprotective crosstalk from vitamin B12 and sphingolipid signaling pathways in therapy for multiple sclerosis.","authors":"Yasuyuki Kihara, Jerold Chun","doi":"10.1093/intimm/dxaf058","DOIUrl":"https://doi.org/10.1093/intimm/dxaf058","url":null,"abstract":"Multiple sclerosis (MS) is an immune-mediated demyelinating disease of the central nervous system (CNS) characterized by neuroinflammation, demyelination, and neurodegeneration. Among disease-modifying therapies (DMTs), sphingosine 1-phosphate (S1P) receptor (S1PR) modulators such as fingolimod, also known as FTY720, have been shown to exert therapeutic effects through direct CNS actions at S1PRs (e.g. S1P1) expressed by astrocytes, beyond the originally proposed mechanism action (MOA) of lymphocyte sequestration. This review highlights the emerging evidence linking S1P signaling to the vitamin B12 pathway, including transcobalamin 2 (TCN2) and CD320. Functional interaction between S1P1 signaling and CD320 expression was discovered by examining gene expression changes in immediate-early astrocytes (ieAstrocytes), the primary CNS cell type activated in response to neuroinflammatory stimuli. This discovery led to the identification of the physical interaction between fingolimod/sphingosine and TCN2 and the potentiation of CD320 internalization by this complex. These findings underscore the importance of CNS vitamin B12 levels in MS and likely other neurological diseases and help to explain the long-appreciated shared neurological symptoms between vitamin B12 deficiency and MS. Future research should investigate therapeutic strategies targeting the crosstalk between the sphingolipid and vitamin B12 pathways to enhance CNS vitamin B12 availability, which can promote neuroprotection in MS and related diseases.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137398","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

The Chitosan Nanoparticle-based Adjuvant CH-100 Orchestrates Multifaceted Innate Immune Activation via STING-Dependent and -Independent Pathways. 壳聚糖纳米颗粒佐剂CH-100通过sting依赖性和非依赖性途径协调多方面的先天免疫激活。

IF 3.2 4区医学

International immunology Pub Date : 2025-09-15 DOI: 10.1093/intimm/dxaf054

Eri Nagai, Daisuke Ori, Norisuke Kano, Moe Ikegawa, Kouji Kobiyama, Ken J Ishii, Takumi Kawasaki, Taro Kawai

{"title":"The Chitosan Nanoparticle-based Adjuvant CH-100 Orchestrates Multifaceted Innate Immune Activation via STING-Dependent and -Independent Pathways.","authors":"Eri Nagai, Daisuke Ori, Norisuke Kano, Moe Ikegawa, Kouji Kobiyama, Ken J Ishii, Takumi Kawasaki, Taro Kawai","doi":"10.1093/intimm/dxaf054","DOIUrl":"https://doi.org/10.1093/intimm/dxaf054","url":null,"abstract":"Adjuvants enhance vaccine efficacy by activating innate immunity, yet the mechanisms of nanoparticle-based adjuvants remain incompletely defined. Here, we characterize CH-100, a chitosan nanoparticle adjuvant, and its capacity to coordinate dendritic cell (DC) activation and promote adaptive immune responses. CH-100 enhances antigen uptake, upregulates co-stimulatory molecules, and elicits antigen-specific antibody and cytotoxic T lymphocytes (CTL) responses. Mechanistically, CH-100 induces mitochondrial ROS, leading to NLRP3 inflammasome activation, although NLRP3 is not essential for the observed adaptive responses. In parallel, CH-100 triggers the STING-IRF3 pathway to induce type I interferons; STING-deficiency partially diminishes antibody and CTL responses, suggesting involvement of additional signaling. Transcriptomic analysis reveals STING-independent upregulation of genes related to Th17 differentiation, accompanied by activation of TBK1, NF-κB, and p38 pathways in DCs, ultimately promoting Th17-skewed immunity. These findings demonstrate how CH-100 engages both STING-dependent and -independent innate pathways to shape adaptive immunity, offering mechanistic insights into chitosan-based adjuvants for future vaccine development.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091609","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

Direct analysis of hepatic stellate cells with flow cytometry in specimens derived from the human liver. 用流式细胞术直接分析人肝脏标本中的肝星状细胞。

IF 3.2 4区医学

International immunology Pub Date : 2025-09-15 DOI: 10.1093/intimm/dxaf055

Toshiaki Bando, Hirotaka Sato, Shunsuke Uno, Hajime Morita, Lynn Zreka, Shuhe Ma, Mouna Khan, Daichi Akuzawa, Yuki Masuo, Joey Matsuyama, Ryo Nishida, Shinya Okumura, Etsuro Hatano, Takashi Ito, Hideki Ueno

{"title":"Direct analysis of hepatic stellate cells with flow cytometry in specimens derived from the human liver.","authors":"Toshiaki Bando, Hirotaka Sato, Shunsuke Uno, Hajime Morita, Lynn Zreka, Shuhe Ma, Mouna Khan, Daichi Akuzawa, Yuki Masuo, Joey Matsuyama, Ryo Nishida, Shinya Okumura, Etsuro Hatano, Takashi Ito, Hideki Ueno","doi":"10.1093/intimm/dxaf055","DOIUrl":"https://doi.org/10.1093/intimm/dxaf055","url":null,"abstract":"Background & aims: Hepatic stellate cells (HSCs) play a crucial role in liver fibrosis. However, the methodology to directly assess the biology of primary HSCs in human liver specimens is yet to be established. In this study, we aimed to establish a robust methodology to analyze primary HSCs in human liver specimens with flow cytometry (FCM).Methods: We first applied FCM to HSCs directly isolated from liver tissues with Nycodenz density gradients. Then, we analyzed HSCs in frozen/thawed liver perfusate samples and liver tissues. We also compared the phenotype of HSCs in primary biliary cholangitis (PBC) and those in healthy counterparts.Results: We found that HSCs were substantially smaller and less dense than normal lymphocytes in the FCM analysis. By carefully defining the FCM gating strategy, we were able to establish the approach to analyze both quiescent HSCs (qHSCs) and activated HSCs (aHSCs) in human liver specimens. Importantly, we found that co-expression of CD14 and CD56 within CD45neg non-immune cells permits the detection of qHSCs, whereas CD68 and CD40 within CD45neg non-immune cells were valuable for assessing aHSCs. Furthermore, we found that aHSCs in PBC upregulated the expression of multiple markers associated with antigen-presentation capacity.Conclusion: Our established approach with FCM will be valuable for the direct analysis of qHSCs and aHSCs with FCM in various human liver specimens. Our FCM analysis of aHSCs in PBC suggested their involvement in the local immune responses.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091642","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

Neuron-microglia interactions modulating neuropathic pain. 神经元-小胶质细胞相互作用调节神经性疼痛。

IF 3.2 4区医学

International immunology Pub Date : 2025-09-10 DOI: 10.1093/intimm/dxaf022

Keita Kohno, Makoto Tsuda

引用次数: 0

The Arf pathway is required for resolving endoplasmic reticulum stress during T-cell activation. 在T细胞活化过程中，Arf通路是解决内质网应激所必需的。

IF 3.2 4区医学

International immunology Pub Date : 2025-09-10 DOI: 10.1093/intimm/dxaf028

Mami Sumiyoshi, Yui Kotani, Chikako Shimokawa, Sukhonthip Khueangchiangkhwang, Yoichi Maekawa, Yoshiyuki Matsuo, Yoshiki Yasukochi, Koichiro Higasa, Yasunori Kanaho, Toshio Watanabe, Satoshi Matsuda

{"title":"The Arf pathway is required for resolving endoplasmic reticulum stress during T-cell activation.","authors":"Mami Sumiyoshi, Yui Kotani, Chikako Shimokawa, Sukhonthip Khueangchiangkhwang, Yoichi Maekawa, Yoshiyuki Matsuo, Yoshiki Yasukochi, Koichiro Higasa, Yasunori Kanaho, Toshio Watanabe, Satoshi Matsuda","doi":"10.1093/intimm/dxaf028","DOIUrl":"10.1093/intimm/dxaf028","url":null,"abstract":"Upon antigen recognition, T cells undergo rapid cell proliferation and differentiation, which is accompanied by a drastic change in cellular metabolism. The ADP-ribosylation factor (Arf) pathway contributes to cellular homeostasis by orchestrating vesicle trafficking, and our previous study using mice lacking both Arf1 and Arf6 (Arf-KO) revealed that Th17-mediated autoimmune diseases were markedly suppressed in Arf-KO mice though the precise mechanism remained elusive. Here, we show that the Arf pathway modulates cellular metabolism in T-cell activation and survival. We found that the lack of Arf1 and Arf6 resulted in hyper-activation of mTOR complex 1 (mTORC1), a master regulator of cellular metabolism, as well as unresolved endoplasmic reticulum (ER) stress, leading to exaggerated apoptosis during T-cell activation. We further demonstrated that treatment with IL-21, a potent inducer of Tfh differentiation, rescued Arf-KO T cells from apoptosis by attenuating ER stress in vitro. Accordingly, antigen-specific antibody production and host defenses against infections such as Leishmania major or Heligmosomoides polygyrus infections were significantly preserved in Arf-KO mice. Taken together, these findings provide mechanistic insights linking the Arf pathway with T-cell homeostasis during activation and identify the Arf pathway as an ideal therapeutic target for autoimmune diseases with a low risk of opportunistic infections.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"611-624"},"PeriodicalIF":3.2,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127626","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

Less severe tumor growth in mice in which mgmt is conditionally deleted using the LysM-Cre system, and the possible impacts of DNA methylation in tumor-associated macrophages. 在使用LysM-Cre系统有条件地删除mgmt的小鼠中较不严重的肿瘤生长，以及肿瘤相关巨噬细胞DNA甲基化的可能影响。

IF 3.2 4区医学

International immunology Pub Date : 2025-09-10 DOI: 10.1093/intimm/dxaf035

Pornpimol Phuengmaung, Wilasinee Saisorn, Atsadang Boonmee, Salisa Benjaskulluecha, Panomwat Amornphimoltham, Arthid Thim-Uam, Tanapat Palaga, Asada Leelahavanichkul

{"title":"Less severe tumor growth in mice in which mgmt is conditionally deleted using the LysM-Cre system, and the possible impacts of DNA methylation in tumor-associated macrophages.","authors":"Pornpimol Phuengmaung, Wilasinee Saisorn, Atsadang Boonmee, Salisa Benjaskulluecha, Panomwat Amornphimoltham, Arthid Thim-Uam, Tanapat Palaga, Asada Leelahavanichkul","doi":"10.1093/intimm/dxaf035","DOIUrl":"10.1093/intimm/dxaf035","url":null,"abstract":"Despite the importance of o6-methylguanine-DNA methyltransferase (MGMT) (a DNA repair enzyme) in cancer cells, the impacts of MGMT in macrophages are still unknown. In mgmt null mice (mgmtflox/flox; LysM-Crecre/-; mgmt deletion only in macrophages), subcutaneous administration of MC38 (a murine colon cancer) induced smaller tumors with lower intratumoral CD206-positive cells (mostly M2-like macrophages) than the tumors in littermate controls (mgmt control) (mgmtfl/fl; LysM-Cre-/-), as indicated by immunohistochemistry and flow cytometry. Then, bone marrow-derived macrophages were incubated with lipopolysaccharide (LPS) (M1 polarization), IL-4 (M2 polarization), MC38-conditioned media (tumor-associated macrophages; TAMs), and control media (control). In comparison with control, mgmt was upregulated in all activated cells (M1, M2, and TAMs), with the most prominent in M1. Less prominent M1 pro-inflammation (lower IL-1β and iNOS expression) and M2 polarization (lower Arg-1 expression) in mgmt null macrophages compared with mgmt control were observed. The tumoricidal activity was demonstrated only in M1 (but not M2 and TAMs), and mgmt control M1 was more prominent than mgmt null M1, as evaluated by flow cytometry using flexible 780 viable dye. There was reduced maximal respiration (extracellular flux analysis) with more prominent cell injuries, as indicated by cell-free DNA, oxidative stress (malondialdehyde), and DNA break (phosphohistone H2AX immunohistochemistry), in TAMs from mgmt null when compared with mgmt control. In conclusion, TAM transformation required cell energy and induced DNA injury, which needed the MGMT enzyme for DNA repair. Without MGMT, the abundance of TAMs was too low to promote cancer growth. The use of MGMT inhibitors for cancers is encouraged.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"635-654"},"PeriodicalIF":3.2,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144266106","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

Correction to: Correlation of interferons and autoimmune aspects in long COVID-19 patients. 修正：长期COVID-19患者中干扰素与自身免疫方面的相关性。

IF 3.2 4区医学

International immunology Pub Date : 2025-09-10 DOI: 10.1093/intimm/dxaf044

引用次数: 0