Immunology & Cell Biology最新文献_第9页

Transcriptional programming governs the transition from shared progenitors to divergent CD8+ T cell fates 转录编程控制着从共享祖细胞到不同CD8+ T细胞命运的转变。

IF 3 4区医学

Immunology & Cell Biology Pub Date : 2026-04-12 Epub Date: 2026-03-11 DOI: 10.1111/imcb.70101

M Zeeshan Chaudhry, Gabrielle T Belz

引用次数: 0

Antigen specificity, not tissue compartment, determines clonal sharing among respiratory tract CD8+ resident memory T cells 抗原特异性，而不是组织区室，决定呼吸道CD8+常驻记忆T细胞之间的克隆共享。

IF 3 4区医学

Immunology & Cell Biology Pub Date : 2026-04-12 Epub Date: 2026-03-02 DOI: 10.1111/imcb.70098

Thi H O Nguyen, Hayley A McQuilten, Angela Pizzolla, Sneha Sant, Kim L Harland, Jessica Braverman, Katherine Kedzierska, Linda M Wakim

{"title":"Antigen specificity, not tissue compartment, determines clonal sharing among respiratory tract CD8+ resident memory T cells","authors":"Thi H O Nguyen, Hayley A McQuilten, Angela Pizzolla, Sneha Sant, Kim L Harland, Jessica Braverman, Katherine Kedzierska, Linda M Wakim","doi":"10.1111/imcb.70098","DOIUrl":"10.1111/imcb.70098","url":null,"abstract":"Tissue-resident memory (Trm) CD8+ T cells in the upper and lower respiratory tract play an instrumental role in combatting influenza virus. While CD8+ Trm populations in these compartments differ in longevity and developmental requirements, it remains unclear whether they share clonotypes, indicating a common origin, or are seeded by distinct T-cell clones. Using a mouse model of influenza virus infection, we investigated the T-cell receptor (TCR) composition of CD8+ Trm specific for two immunodominant influenza-specific CD8+ T-cell epitopes, derived from the nucleoprotein (NP366-374) and polymerase acidic protein (PA224-233). TCRαβ repertoire analysis of NP366-374-specific CD8+ T cells from the nasal mucosa, lung and spleen revealed substantial clonal overlap across resident and circulating subsets, consistent with derivation from a shared precursor pool. In contrast, PA224-233-specific responses showed minimal clonal sharing across tissues and subsets, reflecting a more diverse and private repertoire. Thus, nasal and lung CD8+ Trm can arise from either shared or distinct clonotypes, with their profiles shaped primarily by the antigen specificity rather than tissue location. This allows barrier tissues to be seeded by both highly conserved, public NP366–374-specific CD8+ TCRs and a more diverse, private PA224–233-specific repertoire, together forming an optimal pool capable of providing broadly cross-reactive T-cell immunity and limiting viral escape.","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 4","pages":"358-367"},"PeriodicalIF":3.0,"publicationDate":"2026-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70098","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343090","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

One lineage, many diseases: γδ T cells as context-dependent immune surveyors 一个谱系，多种疾病：γδ T细胞作为环境依赖性免疫测量者。

IF 3 4区医学

Immunology & Cell Biology Pub Date : 2026-04-12 Epub Date: 2026-03-15 DOI: 10.1111/imcb.70103

Lauren J Howson

引用次数: 0

Exploring SIK2-CXCL5 interactions in neutrophils: A novel mechanism for modulating IL-23 and psoriasis progression 探索中性粒细胞中SIK2-CXCL5的相互作用：调节IL-23和牛皮癣进展的新机制。

IF 3 4区医学

Immunology & Cell Biology Pub Date : 2026-04-12 Epub Date: 2026-03-23 DOI: 10.1111/imcb.70105

Yadi Li, Xiaoqian Zhou, Zhusheng Yang, Xiumin Yang, Aihua Wei

{"title":"Exploring SIK2-CXCL5 interactions in neutrophils: A novel mechanism for modulating IL-23 and psoriasis progression","authors":"Yadi Li, Xiaoqian Zhou, Zhusheng Yang, Xiumin Yang, Aihua Wei","doi":"10.1111/imcb.70105","DOIUrl":"10.1111/imcb.70105","url":null,"abstract":"Psoriasis, a chronic inflammatory skin disease, involves dysregulated immune responses and keratinocyte hyperproliferation. The role of salt-inducible kinase 2 (SIK2) in modulating interleukin-23 (IL-23) secretion via C–X–C motif chemokine ligand 5 (CXCL5) in neutrophils has not been fully explored. We combined in vivo and in vitro approaches to examine SIK2's role in an imiquimod (IMQ)-induced psoriasis model and activated neutrophils. Mice underwent intradermal injections of lentiviruses overexpressing SIK2, CXCL5, or both, while in vitro experiments involved transfecting activated neutrophils with these constructs. Assessments included ear thickness, cellular and neutrophil infiltration through histological and immunofluorescence techniques, and analysis of gene and protein expressions via quantitative real-time PCR (qRT-PCR), immunohistochemistry (IHC), and Western blot. Additionally, cell viability, proliferation, and cytokine levels in N-formylmethionyl-leucyl-phenylalanine (fMLF) treated neutrophils were evaluated using cell-counting kit-8 (CCK8), 5-ethynyl-2′-deoxyuridine (EdU) incorporation, and Enzyme-Linked Immunosorbent Assay (ELISA). Overexpression of SIK2 significantly reduced ear thickness, cellular and neutrophil infiltration, IL-1β, tumor necrosis factor-alpha (TNF-α), CXCL5, IL-23 and phosphorylated Yes-associated protein (p-YAP) levels, and increased SIK2 levels in IMQ mice model, but overexpression of CXCL5 reversed these effects. In vitro, SIK2 overexpression resulted in reduced cell viability and proliferation, with corresponding reductions in IL-1β, IL-17, IL-23, and Matrix Metallopeptidase 9 levels, whereas overexpression of CXCL5 reversed these effects. Our findings suggest that SIK2 acts as a critical modulator in psoriasis by influencing CXCL5-mediated IL-23 secretion in neutrophils, underscoring the potential of SIK2 as a therapeutic target to alleviate the inflammatory responses in psoriasis.","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 4","pages":"419-431"},"PeriodicalIF":3.0,"publicationDate":"2026-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147496955","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 NF-κB transcription factor RelA directs mucosal-associated invariant T-cell development NF-κB转录因子RelA指导粘膜相关的不变性t细胞的发育。

IF 3 4区医学

Immunology & Cell Biology Pub Date : 2026-04-12 Epub Date: 2026-02-23 DOI: 10.1111/imcb.70096

Thomas S Fulford, Hui-Fern Koay, Raelene Grumont, Darryl N Johnson, Sebastian Scheer, Hendrik J Nel, Ranjeny Thomas, Jeffrey YW Mak, David P Fairlie, Charis E Teh, Daniel HD Gray, Vanessa L Bryant, Colby Zaph, Lorraine A O'Reilly, Steven Gerondakis, Dale I Godfrey

{"title":"The NF-κB transcription factor RelA directs mucosal-associated invariant T-cell development","authors":"Thomas S Fulford, Hui-Fern Koay, Raelene Grumont, Darryl N Johnson, Sebastian Scheer, Hendrik J Nel, Ranjeny Thomas, Jeffrey YW Mak, David P Fairlie, Charis E Teh, Daniel HD Gray, Vanessa L Bryant, Colby Zaph, Lorraine A O'Reilly, Steven Gerondakis, Dale I Godfrey","doi":"10.1111/imcb.70096","DOIUrl":"10.1111/imcb.70096","url":null,"abstract":"Mucosal-associated invariant T (MAIT) cells are characterized by rapid responses to nonpeptide antigens via invariant T-cell receptors (TCR), and expression of an “effector-like” T-cell phenotype. The transcription factor promyelocytic leukemia zinc finger (PLZF) is crucial for defining the function of MAIT cells and other unconventional T cells; however, the transcriptional programs that direct MAIT cell development are not fully elucidated. Here, we show that the canonical NF-κB transcription factor RelA is critical for MAIT cell thymic development, but not responsiveness to antigen, whereas NF-κB1 and c-Rel make more limited contributions. MAIT cell development is also impaired in the absence of the linear ubiquitin signaling complex (LUBAC), an upstream regulator of NF-κB signaling, implicating this pathway in establishing the MAIT cell pool. Collectively, these data suggest LUBAC and NF-κB signals as elements of the transcriptional network controlling MAIT cell development.","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 4","pages":"329-344"},"PeriodicalIF":3.0,"publicationDate":"2026-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70096","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147275251","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

Innate lymphoid cells at the heart of the enteric neuroimmune system 先天淋巴样细胞是肠道神经免疫系统的核心。

IF 3 4区医学

Immunology & Cell Biology Pub Date : 2026-04-12 Epub Date: 2026-03-08 DOI: 10.1111/imcb.70100

Cyril Seillet

引用次数: 0

IF 3 4区医学

Immunology & Cell Biology Pub Date : 2026-04-12 Epub Date: 2026-03-12 DOI: 10.1111/imcb.70102

Shivali Savita Chinni, Gemma S Trollope, Patrick Leung, Jonathan L McQualter, Chee Wah Tan, Linfa Wang, Leonard Lim, Adam K Wheatley, Jennifer A Juno, Stephen J Kent, Hareth A Al-Wassiti, Colin W Pouton, Kylie M Quinn

{"title":"Age-related differences in mRNA vaccine immunogenicity and adjuvancy","authors":"Shivali Savita Chinni, Gemma S Trollope, Patrick Leung, Jonathan L McQualter, Chee Wah Tan, Linfa Wang, Leonard Lim, Adam K Wheatley, Jennifer A Juno, Stephen J Kent, Hareth A Al-Wassiti, Colin W Pouton, Kylie M Quinn","doi":"10.1111/imcb.70102","DOIUrl":"10.1111/imcb.70102","url":null,"abstract":"Older people mount poorer adaptive immune responses to mRNA vaccines, leaving them more vulnerable to infection with SARS-CoV-2. To design better mRNA vaccines for older people, we need to understand how aging alters mechanisms of adjuvancy that shape immunogenicity. To first define age-related changes in immunogenicity, we vaccinated young (< 5 months old) and aged (> 18 months old) C57BL/6 mice with an mRNA vaccine encoding the SARS-CoV-2 spike protein. T cell responses were markedly reduced in aged mice at peak and memory timepoints, using intracellular cytokine staining or activation-induced marker assays. Spike and receptor-binding domain binding and neutralizing antibody titers were also markedly reduced in aged mice, consistent with deficits seen in older humans. To define age-related changes in adjuvancy mechanisms, we vaccinated young and aged mice with mRNA vaccines loaded with DiD lipid dye or mScarlet mRNA, then tracked dendritic cell (DC) numbers, phenotype, vaccine uptake, antigen expression, and activation, as well as local and systemic cytokine production. DC numbers in the draining lymph nodes (dLN) were dramatically reduced before and early after vaccination in aged compared to young mice, with delayed recruitment of DCs to the dLN. Vaccine uptake was not impacted by age, but the frequency of DCs expressing antigen increased with age and DC activation decreased with age. Aging accelerated the expression of some cytokines (IL-1α, IL-6), while delaying others (IFNγ, MCP-1) in dLNs and sera. This illustrates that aging impairs multiple adjuvancy mechanisms but mRNA vaccine strategies that address these age-related deficits could improve responses in older people.","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 4","pages":"400-414"},"PeriodicalIF":3.0,"publicationDate":"2026-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70102","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147442016","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

C3AR1 regulates intestinal T-cell immune response after burn by activating the NF-κB signaling pathway C3AR1通过激活NF-κB信号通路调控烧伤后肠道t细胞免疫应答。

IF 3 4区医学

Immunology & Cell Biology Pub Date : 2026-04-12 Epub Date: 2026-02-27 DOI: 10.1111/imcb.70099

Jingyu Wei, Kai Zhang, Weicheng Pan, Yunjian Li, Qiang Shi, Yun Cheng, Wenwen Zhang

{"title":"C3AR1 regulates intestinal T-cell immune response after burn by activating the NF-κB signaling pathway","authors":"Jingyu Wei, Kai Zhang, Weicheng Pan, Yunjian Li, Qiang Shi, Yun Cheng, Wenwen Zhang","doi":"10.1111/imcb.70099","DOIUrl":"10.1111/imcb.70099","url":null,"abstract":"Severe burns are characterized by high mortality and morbidity rates. Immune dysfunction during the acute phase of severe burns exacerbates tissue damage. Complement C3a receptor 1 (C3AR1) is a key receptor associated with severe burn shock. This study aimed to investigate the effects of C3AR1 on T-cell immunity in the intestine following burns. We established a mouse model of severe burns and performed in vitro stimulation of CD3+ T cells with C3AR1 agonist. Quantitative real-time PCR, Western blot, ELISA, and flow cytometry were used to analyze the expression of C3AR1, IL-2, IL-10 and factors related to the NF-κB signaling pathway, changes in the proportions of Th1 and Th2 subsets, and the apoptosis rate of CD3+ T cells after C3AR1 stimulation. The results showed that C3AR1 expression in the intestinal mucosa of severely burned mice was significantly elevated, while IL-2 expression was decreased, exhibiting a negative correlation. After C3AR1 overexpression, the proportion of Th1 cells decreased, the apoptosis rates of Th2 cells and CD3+ T cells increased, IL-2 expression was reduced, and the NF-κB signaling pathway was activated. In conclusion, C3AR1 participates in intestinal T-cell immune responses after burns through activation of the NF-κB signaling pathway, indicating that C3AR1 is a crucial regulator in the recovery of intestinal mucosal injury and immune function balance, and may serve as a potential molecular target for burn treatment.","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 4","pages":"345-357"},"PeriodicalIF":3.0,"publicationDate":"2026-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147315918","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 role of peripheral serotonin in SARS-CoV-2 infectivity, COVID-19 treatment and long COVID 外周血清素在SARS-CoV-2感染、COVID-19治疗和长期COVID中的作用。

IF 3 4区医学

Immunology & Cell Biology Pub Date : 2026-04-12 Epub Date: 2026-03-08 DOI: 10.1111/imcb.70097

Daniel W Thorpe, Lauren A Jones, Alyce M Martin, Rosemary A Coleman, Caitlin Allman, Rochelle A Peterson, Damien J Keating

{"title":"The role of peripheral serotonin in SARS-CoV-2 infectivity, COVID-19 treatment and long COVID","authors":"Daniel W Thorpe, Lauren A Jones, Alyce M Martin, Rosemary A Coleman, Caitlin Allman, Rochelle A Peterson, Damien J Keating","doi":"10.1111/imcb.70097","DOIUrl":"10.1111/imcb.70097","url":null,"abstract":"Gastrointestinal symptoms have emerged as a common, but underappreciated, cause of morbidity in relation to SARS-CoV-2 infection and the COVID-19 pandemic. This manifests as a range of indications including diarrhea, anorexia, nausea, vomiting and abdominal pain. In addition, the gastrointestinal tract may represent a route of viral entry via the epithelial cell layer lining the gut wall. This route of entry could be a significant component of disease pathogenesis, including effects on the nervous system via the gut-brain axis. In this review, we provide an assessment of the effects of COVID-19 on the gastrointestinal system, its involvement in disease severity and potential pathways for viral entry and infection in the gastrointestinal tract. We also examine evidence that gut-derived serotonin is affected by SARS-CoV-2 infection, how this may link to symptoms and disease pathogenesis and the potential link to the efficacy of selective serotonin reuptake inhibitors in reducing COVID-19 severity.","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 4","pages":"368-376"},"PeriodicalIF":3.0,"publicationDate":"2026-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70097","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147375538","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

IF 3 4区医学

Immunology & Cell Biology Pub Date : 2026-04-10

引用次数: 0