Journal of immunology最新文献_第4页

TLR7-Induced Mitochondrial Reactive Oxygen Species Production in Monocyte-derived Dendritic Cells Drives IL-12-Dependent NK Cell Activation and Enhances Antitumor Immunity. 单核细胞衍生树突状细胞中 TLR7 诱导的线粒体活性氧生成驱动 IL-12 依赖性 NK 细胞活化并增强抗肿瘤免疫力

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-09-06 DOI: 10.4049/jimmunol.2400340

Ankush Paladhi, Samrat Daripa, Arghya Nath, Sumit Kumar Hira

引用次数: 0

Ebi3 Binding to IFN-γ and IL-10 Limits Their Function. Ebi3 与 IFN-γ 和 IL-10 的结合限制了它们的功能。

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-09-06 DOI: 10.4049/jimmunol.2400236

Ellen N Scott, Cheng Ye, Hiroshi Yano, Zhanna Lipatova, Erin Brunazzi, Kate M Vignali, Creg J Workman, Dario A A Vignali

{"title":"Ebi3 Binding to IFN-γ and IL-10 Limits Their Function.","authors":"Ellen N Scott, Cheng Ye, Hiroshi Yano, Zhanna Lipatova, Erin Brunazzi, Kate M Vignali, Creg J Workman, Dario A A Vignali","doi":"10.4049/jimmunol.2400236","DOIUrl":"10.4049/jimmunol.2400236","url":null,"abstract":"EBV-induced gene 3 (Ebi3) is a β subunit within the IL-12 cytokine family that canonically binds to α subunits p19, p28, or p35 to form the heterodimeric cytokines IL-39, IL-27, and IL-35, respectively. In the last decade, the binding partners for Ebi3 have continued to expand to include IL-6 and the other IL-12 family β subunit p40, revealing the possibility that Ebi3 may be able to bind to other cytokines and have distinct functions. We first explored this possibility utilizing an in vivo mouse model of regulatory T cell-restricted deletions of the subunits composing the cytokine IL-35, p35, and Ebi3, and we observed a differential impact on CD8+ T cell inhibitory receptor expression despite comparable reduction in tumor growth. We then screened the ability of Ebi3 to bind to different cytokines with varying structural resemblance to the IL-12 family α subunits. These in vitro screens revealed extracellular binding of Ebi3 to both IFN-γ and IL-10. Ebi3 bound to IFN-γ and IL-10 abrogated signal transduction and downstream functions of both cytokines. Lastly, we validated that extracellular complex formation after mixing native proteins resulted in loss of function. These data suggest that secreted partnerless Ebi3 may bind to cytokines within the extracellular microenvironment and act as a cytokine sink, further expanding the potential immunological impact of Ebi3.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142140267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

MAFB in Macrophages Regulates Prostaglandin E2-Mediated Lipid Mediator Class Switch through ALOX15 in Ischemic Acute Kidney Injury. 缺血性急性肾损伤中巨噬细胞中的 MAFB 通过 ALOX15 调控前列腺素 E2 介导的脂质介质类别转换

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-09-04 DOI: 10.4049/jimmunol.2300844

Maho Kanai, Teppei Nishino, Dhouha Daassi, Akari Kimura, Ching-Wei Liao, Zeynab Javanfekr Shahri, Arata Wakimoto, Natalia Gogoleva, Toshiaki Usui, Naoki Morito, Makoto Arita, Satoru Takahashi, Michito Hamada

{"title":"MAFB in Macrophages Regulates Prostaglandin E2-Mediated Lipid Mediator Class Switch through ALOX15 in Ischemic Acute Kidney Injury.","authors":"Maho Kanai, Teppei Nishino, Dhouha Daassi, Akari Kimura, Ching-Wei Liao, Zeynab Javanfekr Shahri, Arata Wakimoto, Natalia Gogoleva, Toshiaki Usui, Naoki Morito, Makoto Arita, Satoru Takahashi, Michito Hamada","doi":"10.4049/jimmunol.2300844","DOIUrl":"https://doi.org/10.4049/jimmunol.2300844","url":null,"abstract":"Monocytes and macrophages express the transcription factor MAFB (V-maf musculoaponeurotic fibrosarcoma oncogene homolog B) and protect against ischemic acute kidney injury (AKI). However, the mechanism through which MAFB alleviates AKI in macrophages remains unclear. In this study, we induced AKI in macrophage lineage-specific Mafb-deficient mice (C57BL/6J) using the ischemia-reperfusion injury model to analyze these mechanisms. Our results showed that MAFB regulates the expression of Alox15 (arachidonate 15-lipoxygenase) in macrophages during ischemic AKI. The expression of ALOX15 was significantly decreased at the mRNA and protein levels in macrophages that infiltrated the kidneys of macrophage-specific Mafb-deficient mice at 24 h after ischemia-reperfusion injury. ALOX15 promotes the resolution of inflammation under acute conditions by producing specialized proresolving mediators by oxidizing essential fatty acids. Therefore, MAFB in macrophages promotes the resolution of inflammation in ischemic AKI by regulating the expression of Alox15. Moreover, MAFB expression in macrophages is upregulated via the COX-2/PGE2/EP4 pathway in ischemic AKI. Our in vitro assay showed that MAFB regulates the expression of Alox15 under the COX-2/PGE2/EP4 pathway in macrophages. PGE2 mediates the lipid mediator (LM) class switch from inflammatory LMs to specialized proresolving mediators. Therefore, MAFB plays a key role in the PGE2-mediated LM class switch by regulating the expression of Alox15. Our study identified a previously unknown mechanism by which MAFB in macrophages alleviates ischemic AKI and provides new insights into regulating the LM class switch in acute inflammatory conditions.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142125948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Potential Contributions of Human Endogenous Retroviruses in Innate Immune Memory. 人类内源性逆转录病毒在先天性免疫记忆中的潜在贡献

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-09-04 DOI: 10.4049/jimmunol.2300411

Pengcheng Du, Jiarui Li, Mingxi Hua, Liuluan Zhu, Chen Chen, Hui Zeng

{"title":"Potential Contributions of Human Endogenous Retroviruses in Innate Immune Memory.","authors":"Pengcheng Du, Jiarui Li, Mingxi Hua, Liuluan Zhu, Chen Chen, Hui Zeng","doi":"10.4049/jimmunol.2300411","DOIUrl":"https://doi.org/10.4049/jimmunol.2300411","url":null,"abstract":"The phenomenon wherein innate immune cells adopt long-term inflammatory phenotypes following the first stimuli is named trained immunity and can improve host defense against infections. Transcriptional and epigenetic reprogramming are critical mechanisms of trained immunity; however, the regulatory networks are not entirely clear at present. The human endogenous retroviruses (HERVs) provide large amounts of transcriptional regulators in the regulatory pathways. In this study, we analyzed published large omics data to explore the roles of such \"dark matter\" of the human genome in trained and tolerant macrophages. We collected 80 RNA sequencing data and 62 sequencing data to detect histone modifications and active regulatory regions from nine published studies on trained and tolerant macrophages. By analyzing the characteristics of transcription and epigenetic modification of HERVs, as well as their association with gene expression, we found that 15.3% of HERVs were transcribed nonrandomly from noncoding regions and enriched in specific HERV families and specific chromosomes, such as chromosomes 11, 15, 17, and 19, and they were highly related with the expression of adjacent genes. We found that 295 differentially expressed HERVs are located in 50-kbp flanking regions of 142 differentially expressed genes. We found epigenetic changes of these HERVs and that overlap with predicted enhancers and identified 35 enhancer-like HERVs. The related genes were highly involved in the activation and inflammatory responses, such as the TLR pathway. Other pathways including phosphoinositide signaling and transport of folate and K+ might be also related with trained immunity, which require further study. These results demonstrated that HERVs might play important roles in trained immunity.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142125949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Mycobacterium tuberculosis Utilizes Serine/Threonine Kinase PknF to Evade NLRP3 Inflammasome-driven Caspase-1 and RIPK3/Caspase-8 Activation in Murine Dendritic Cells. 结核分枝杆菌利用丝氨酸/苏氨酸激酶 PknF 回避小鼠树突状细胞中 NLRP3 炎症体驱动的 Caspase-1 和 RIPK3/Caspase-8 激活。

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-09-01 DOI: 10.4049/jimmunol.2300753

Shivangi Rastogi, Akshaya Ganesh, Volker Briken

{"title":"Mycobacterium tuberculosis Utilizes Serine/Threonine Kinase PknF to Evade NLRP3 Inflammasome-driven Caspase-1 and RIPK3/Caspase-8 Activation in Murine Dendritic Cells.","authors":"Shivangi Rastogi, Akshaya Ganesh, Volker Briken","doi":"10.4049/jimmunol.2300753","DOIUrl":"10.4049/jimmunol.2300753","url":null,"abstract":"Dendritic cells (DCs) are crucial for initiating the acquired immune response to infectious diseases such as tuberculosis. Mycobacterium tuberculosis has evolved strategies to inhibit activation of the NLRP3 inflammasome in macrophages via its serine/threonine protein kinase, protein kinase F (PknF). It is not known whether this pathway is conserved in DCs. In this study, we show that the pknF deletion mutant of M. tuberculosis (MtbΔpknF) compared with wild-type M. tuberculosis-infected cells induces increased production of IL-1β and increased pyroptosis in murine bone marrow-derived DCs (BMDCs). As shown for murine macrophages, the enhanced production of IL-1β postinfection of BMDCs with MtbΔpknF is dependent on NLRP3, ASC, and caspase-1/11. In contrast to macrophages, we show that MtbΔpknF mediates RIPK3/caspase-8-dependent IL-1β production in BMDCs. Consistently, infection with MtbΔpknF results in increased activation of caspase-1 and caspase-8 in BMDCs. When compared with M. tuberculosis-infected cells, the IL-6 production by MtbΔpknF-infected cells was unchanged, indicating that the mutant does not affect the priming phase of inflammasome activation. In contrast, the activation phase was impacted because the MtbΔpknF-induced inflammasome activation in BMDCs depended on potassium efflux, chloride efflux, reactive oxygen species generation, and calcium influx. In conclusion, PknF is important for M. tuberculosis to evade NLRP3 inflammasome-mediated activation of caspase-1 and RIPK3/caspase-8 pathways in BMDCs.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141633692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 Crystal Structure of the Michaelis-Menten Complex of C1 Esterase Inhibitor and C1s Reveals Novel Insights into Complement Regulation. C1 酯酶抑制剂和 C1s 的 Michaelis-Menten 复合物晶体结构揭示了补体调节的新观点。

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-09-01 DOI: 10.4049/jimmunol.2400194

Ryan J Garrigues, Matthew P Garrison, Brandon L Garcia

{"title":"The Crystal Structure of the Michaelis-Menten Complex of C1 Esterase Inhibitor and C1s Reveals Novel Insights into Complement Regulation.","authors":"Ryan J Garrigues, Matthew P Garrison, Brandon L Garcia","doi":"10.4049/jimmunol.2400194","DOIUrl":"10.4049/jimmunol.2400194","url":null,"abstract":"The ancient arm of innate immunity known as the complement system is a blood proteolytic cascade involving dozens of membrane-bound and solution-phase components. Although many of these components serve as regulatory molecules to facilitate controlled activation of the cascade, C1 esterase inhibitor (C1-INH) is the sole canonical complement regulator belonging to a superfamily of covalent inhibitors known as serine protease inhibitors (SERPINs). In addition to its namesake role in complement regulation, C1-INH also regulates proteases of the coagulation, fibrinolysis, and contact pathways. Despite this, the structural basis for C1-INH recognition of its target proteases has remained elusive. In this study, we present the crystal structure of the Michaelis-Menten (M-M) complex of the catalytic domain of complement component C1s and the SERPIN domain of C1-INH at a limiting resolution of 3.94 Å. Analysis of the structure revealed that nearly half of the protein/protein interface is formed by residues outside of the C1-INH reactive center loop. The contribution of these residues to the affinity of the M-M complex was validated by site-directed mutagenesis using surface plasmon resonance. Parallel analysis confirmed that C1-INH-interfacing residues on C1s surface loops distal from the active site also drive affinity of the M-M complex. Detailed structural comparisons revealed differences in substrate recognition by C1s compared with C1-INH recognition and highlight the importance of exosite interactions across broader SERPIN/protease systems. Collectively, this study improves our understanding of how C1-INH regulates the classical pathway of complement, and it sheds new light on how SERPINs recognize their cognate protease targets.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11333171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

IL-27 Gene Therapy Ameliorates IPEX Syndrome Caused by Germline Mutation of Foxp3 Gene: A Major Role for Induction of IL-10. IL-27基因疗法可改善Foxp3基因种系突变引起的IPEX综合征：IL-10的诱导起主要作用。

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-09-01 DOI: 10.4049/jimmunol.2400056

Jin-Qing Liu, Ali Jabbari, Cho-Hao Lin, Venu Akkanapally, Wendy L Frankel, Sujit Basu, Kai He, Pan Zheng, Yang Liu, Xue-Feng Bai

{"title":"IL-27 Gene Therapy Ameliorates IPEX Syndrome Caused by Germline Mutation of Foxp3 Gene: A Major Role for Induction of IL-10.","authors":"Jin-Qing Liu, Ali Jabbari, Cho-Hao Lin, Venu Akkanapally, Wendy L Frankel, Sujit Basu, Kai He, Pan Zheng, Yang Liu, Xue-Feng Bai","doi":"10.4049/jimmunol.2400056","DOIUrl":"10.4049/jimmunol.2400056","url":null,"abstract":"Inactivating mutations of Foxp3, the master regulator of regulatory T cell development and function, lead to immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome in mice and humans. IPEX is a fatal autoimmune disease, with allogeneic stem cell transplant being the only available therapy. In this study, we report that a single dose of adeno-associated virus (AAV)-IL-27 to young mice with naturally occurring Foxp3 mutation (Scurfy mice) substantially ameliorates clinical symptoms, including growth retardation and early fatality. Correspondingly, AAV-IL-27 gene therapy significantly prevented naive T cell activation, as manifested by downregulation of CD62L and upregulation of CD44, and immunopathology typical of IPEX. Because IL-27 is known to induce IL-10, a key effector molecule of regulatory T cells, we evaluated the contribution of IL-10 induction by crossing IL-10-null allele to Scurfy mice. Although IL-10 deficiency does not affect the survival of Scurfy mice, it largely abrogated the therapeutic effect of AAV-IL-27. Our study revealed a major role for IL-10 in AAV-IL-27 gene therapy and demonstrated that IPEX is amenable to gene therapy.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11333164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

TLR10 (CD290) Is a Regulator of Immune Responses in Human Plasmacytoid Dendritic Cells. TLR10（CD290）是人类浆细胞树突状细胞免疫反应的调节因子

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-09-01 DOI: 10.4049/jimmunol.2200468

Pratik Deb, Sukhwinder Singh, Evelyne Kalyoussef, Nicholas J Hess, Richard I Tapping, Patricia Fitzgerald-Bocarsly

{"title":"TLR10 (CD290) Is a Regulator of Immune Responses in Human Plasmacytoid Dendritic Cells.","authors":"Pratik Deb, Sukhwinder Singh, Evelyne Kalyoussef, Nicholas J Hess, Richard I Tapping, Patricia Fitzgerald-Bocarsly","doi":"10.4049/jimmunol.2200468","DOIUrl":"10.4049/jimmunol.2200468","url":null,"abstract":"TLRs are the most thoroughly studied group of pattern-recognition receptors that play a central role in innate immunity. Among them, TLR10 (CD290) remains the only TLR family member without a known ligand and clearly defined functions. One major impediment to studying TLR10 is its absence in mice. A recent study on TLR10 knock-in mice demonstrated its intrinsic inhibitory role in B cells, indicating that TLR10 is a potential drug target in autoimmune diseases. In this study, we interrogated the expression and function of TLR10 in human plasmacytoid dendritic cells (pDCs). We have seen that primary human pDCs, B cells, and monocytes constitutively express TLR10. Upon preincubation with an anti-TLR10 Ab, production of cytokines in pDCs was downregulated in response to stimulation with DNA and RNA viruses. Upon further investigation into the possible mechanism, we documented phosphorylation of STAT3 upon Ab-mediated engagement of TLR10. This leads to the induction of inhibitory molecule suppressor of cytokine signaling 3 (SOCS3) expression. We have also documented the inhibition of nuclear translocation of transcription factor IFN regulatory factor 7 (IRF7) in pDCs following TLR10 engagement. Our data provide the (to our knowledge) first evidence that TLR10 is constitutively expressed on the surface of human pDCs and works as a regulator of their innate response. Our findings indicate the potential of harnessing the function of pDCs by Ab-mediated targeting of TLR10 that may open a new therapeutic avenue for autoimmune disorders.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11333166/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Lung-resident CD3-NK1.1+CD69+CD103+ Cells Play an Important Role in Bacillus Calmette-Guérin Vaccine-Induced Protective Immunity against Mycobacterium tuberculosis Infection. 肺驻留 CD3-NK1.1+CD69+CD103+ 细胞在卡介苗诱导的结核分枝杆菌感染保护性免疫中发挥重要作用

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-09-01 DOI: 10.4049/jimmunol.2200728

Olamipejo Durojaye, Abhinav Vankayalapati, Padmaja Paidipally, Tanmoy Mukherjee, Ramakrishna Vankayalapati, Rajesh Kumar Radhakrishnan

{"title":"Lung-resident CD3-NK1.1+CD69+CD103+ Cells Play an Important Role in Bacillus Calmette-Guérin Vaccine-Induced Protective Immunity against Mycobacterium tuberculosis Infection.","authors":"Olamipejo Durojaye, Abhinav Vankayalapati, Padmaja Paidipally, Tanmoy Mukherjee, Ramakrishna Vankayalapati, Rajesh Kumar Radhakrishnan","doi":"10.4049/jimmunol.2200728","DOIUrl":"10.4049/jimmunol.2200728","url":null,"abstract":"Tissue-resident immune cells play important roles in local tissue homeostasis and infection control. There is no information on the functional role of lung-resident CD3-NK1.1+CD69+CD103+ cells in intranasal Bacillus Calmette-Guérin (BCG)-vaccinated and/or Mycobacterium tuberculosis (Mtb)-infected mice. Therefore, we phenotypically and functionally characterized these cells in mice vaccinated intranasally with BCG. We found that intranasal BCG vaccination increased CD3-NK1.1+ cells with a tissue-resident phenotype (CD69+CD103+) in the lungs during the first 7 d after BCG vaccination. Three months post-BCG vaccination, Mtb infection induced the expansion of CD3-NK1.1+CD69+CD103+ (lung-resident) cells in the lung. Adoptive transfer of lung-resident CD3-NK1.1+CD69+CD103+ cells from the lungs of BCG-vaccinated mice to Mtb-infected naive mice resulted in a lower bacterial burden and reduced inflammation in the lungs. Our findings demonstrated that intranasal BCG vaccination induces the expansion of CD3-NK1.1+CD69+CD103+ (lung-resident) cells to provide protection against Mtb infection.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141616661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Cutting Edge: Redundant Roles for MHC Class II-, CD1d-, and MR1-restricted T Cells in Clearing Bartonella Infection. 前沿：MHC II 类、CD1d 和 MR1 限制性 T 细胞在清除巴顿氏菌感染中的冗余作用。

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-09-01 DOI: 10.4049/jimmunol.2400045

Lena K Siewert, Katja Fromm, Christoph Dehio, Daniel D Pinschewer

{"title":"Cutting Edge: Redundant Roles for MHC Class II-, CD1d-, and MR1-restricted T Cells in Clearing Bartonella Infection.","authors":"Lena K Siewert, Katja Fromm, Christoph Dehio, Daniel D Pinschewer","doi":"10.4049/jimmunol.2400045","DOIUrl":"10.4049/jimmunol.2400045","url":null,"abstract":"The importance of unconventional T cells for mucosal immunity is firmly established but for systemic bacterial infection remains less well defined. In this study, we explored the role of various T cell subsets in murine Bartonella infection, which establishes persistent bacteremia unless controlled by antibacterial Abs. We found that αβ T cells are essential for Ab production against and clearance of B. taylorii, whereas MHC class I (MHC-I)- or MHC class II (MHC-II)-deficient mice eliminated B. taylorii infection with normal kinetics. Similarly, animals lacking either CD1d or MR1 suppressed bacteremia with normal kinetics. Interestingly, mice with a combined deficiency of either MHC-II and CD1d or MHC-II and MR1 failed to clear the infection, indicating that the combination of CD1d- and MR1-restricted T cells can compensate for the lack of MHC-II in this model. Our data document a previously underappreciated contribution of unconventional T cells to the control of systemic bacterial infection, supposedly as helper cells for antibacterial Ab production.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11335324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141563510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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