ImmunoHorizons最新文献_第4页

Neurogranin negatively regulates gene expression and proinflammatory mediator release in allergen-activated mast cells. 神经粒蛋白负调控基因表达和促炎介质释放在过敏原激活肥大细胞。

ImmunoHorizons Pub Date : 2026-05-13 DOI: 10.1093/immhor/vlag026

Katie D Hunter, Robert W E Crozier, Ryan W Baranowski, Val A Fajardo, Adam J MacNeil

{"title":"Neurogranin negatively regulates gene expression and proinflammatory mediator release in allergen-activated mast cells.","authors":"Katie D Hunter, Robert W E Crozier, Ryan W Baranowski, Val A Fajardo, Adam J MacNeil","doi":"10.1093/immhor/vlag026","DOIUrl":"10.1093/immhor/vlag026","url":null,"abstract":"Mast cells are critical players in the maladaptive immune responses underlying biphasic reactions in allergic inflammation. Neurogranin (Ng) is an IQ domain-containing protein that sequesters Calmodulin under low [Ca2+] and negatively regulates calmodulin-mediated signaling such as calcineurin activation, in addition to downstream inflammatory responses. Previously described as brain specific, Ng has recently been identified in the spleen, bone marrow, and B lymphocytes, highlighting the need to investigate its negative regulatory role in other proinflammatory contexts. Here, we sought to determine the role of Ng in allergen-activated mast cells, to better understand the negative regulatory mechanisms that can potentially be exploited to help alleviate the severity of allergic inflammation. Using bone marrow-derived mast cells from wild-type (Nrgn+/+) and heterozygous (Nrgn+/-) mice, we identified that Ng is present in mast cells. It was determined that although Ng did not influence the development of mature mast cells or the extent of early-phase inflammation, a reduction in Ng significantly increased gene expression of IL6 and IL13, which was coupled with an increase in release of IL-6, IL-13, TNF, CCL1, CCL2, and CCL3. Together, this is the first study to identify Ng in mast cells, in addition to positioning its role as a negative regulator of mast cell responses following allergen activation. These data highlight the need for future research to further elucidate the role of Ng in IgE-mediated mast cell activation to better understand the regulatory mechanisms of these inflammatory cells in mast cell-driven normal and pathological contexts.","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 5","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13218791/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148059157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The influence of exercise modality on the inflammatory response to high-intensity interval training. 运动方式对高强度间歇训练炎症反应的影响。

ImmunoHorizons Pub Date : 2026-05-13 DOI: 10.1093/immhor/vlag022

Juliet Moore, Jonathan Katz, George Salem

{"title":"The influence of exercise modality on the inflammatory response to high-intensity interval training.","authors":"Juliet Moore, Jonathan Katz, George Salem","doi":"10.1093/immhor/vlag022","DOIUrl":"10.1093/immhor/vlag022","url":null,"abstract":"The effect of exercise on immune system activation and regulation has been well studied in athletes following long-duration exercise and elite events, and across various modalities; however, little work has been performed using shorter-duration, high-intensity protocols and in recreational athletes. This study examined the comparative effects of both treadmill running and stationary cycling, high-intensity interval training (HIIT) on circulating inflammatory biomarkers. A total of 26 young, healthy participants completed both exercise modality protocols in a randomized order using a crossover design. Blood samples were collected at baseline, immediately after exercise, and 1 and 24 h postexercise time points, then processed for cytokine concentrations. Interleukin (IL)-6 increased immediately following both exercise modalities (P < 0.001). IL-8 increased following treadmill running (P = 0.02) and continued to increase during 1 h and 24 h recovery postexercise (P < 0.001). IL-10 increased following 24 h recovery in treadmill running (P < 0.01) and stationary cycling (P < 0.05). There were no significant changes in IL-1ra or tumor necrosis factor α. C-reactive protein trended to increase 24 h after treadmill running with a large effect size (η2 = 0.22). Treadmill running and stationary cycling HIIT provide the necessary stimulus to alter circulating cytokine concentrations. IL-6 and IL-10 increased to the same extent following both exercise modalities. IL-8 was found to increase significantly following treadmill HIIT but not following cycling HIIT. These findings may inform the design of future studies investigating the influence of HIIT on measures of inflammation and health in healthy and clinical populations.","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 5","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13215878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148044450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to: A widely used EYFP-based CRE reporter Mouse Line fails to detect a significant fraction of CRE+ T cells. 更正：广泛使用的基于eyfp的CRE报告小鼠系未能检测到相当一部分CRE+ T细胞。

ImmunoHorizons Pub Date : 2026-05-13 DOI: 10.1093/immhor/vlag017

引用次数: 0

RANKL inhibits macrophage proinflammatory Toll-like receptor 2 and 4 signaling and impairs killing of intracellular bacteria. RANKL抑制巨噬细胞促炎toll样受体2和4信号，损害细胞内细菌的杀伤。

ImmunoHorizons Pub Date : 2026-05-13 DOI: 10.1093/immhor/vlag023

Clara D Si, Christopher T Peek, Sana R Fatah, Andrew J Beaudoin, Anton R Zhelonkin, Kara R Eichelberger, Stacy L Hahn, Robert O Watson, Denis A Mogilenko, James E Cassat

{"title":"RANKL inhibits macrophage proinflammatory Toll-like receptor 2 and 4 signaling and impairs killing of intracellular bacteria.","authors":"Clara D Si, Christopher T Peek, Sana R Fatah, Andrew J Beaudoin, Anton R Zhelonkin, Kara R Eichelberger, Stacy L Hahn, Robert O Watson, Denis A Mogilenko, James E Cassat","doi":"10.1093/immhor/vlag023","DOIUrl":"10.1093/immhor/vlag023","url":null,"abstract":"Monocyte-macrophage lineage cells, crucial components of the innate immune system, can uniquely form bone-resorbing osteoclasts upon exposure to the cytokine receptor activator of nuclear factor κB ligand (RANKL) in the bone microenvironment. Recent studies have also begun to uncover extensive extraskeletal roles of RANKL. However, how monocyte-macrophage lineage cells respond to RANKL outside of the bone, and the impact that this signaling pathway exerts on the host immune response, is not fully understood. In this study, we sought to define how RANKL exposure shapes the macrophage inflammatory response to pathogens by using the model intracellular bacterium Salmonella enterica serovar Typhimurium, which coopts macrophages to cause life-threatening infections. We found that exposing both mouse and human macrophages to subosteoclastogenic levels of RANKL increased intracellular Salmonella enterica serovar Typhimurium burdens and decreased proinflammatory cytokine production. RNA sequencing revealed downregulation of pattern recognition receptor signaling pathways in RANKL-treated macrophages during the early stages of infection. Therefore, we hypothesized that RANKL impairs pattern recognition receptor-dependent signaling pathways that are important for proinflammatory cytokine production. We discovered that RANKL-treated macrophages exhibit reduced nuclear factor κB and interferon regulatory factor 3 activation, specifically in response to Toll-like receptor 2 (TLR2) and TLR4 stimulation. We determined that prior RANKL exposure decreases abundance of the TLR2 and TLR4 adaptor proteins TRAM (TRIF-related adaptor molecule) and TIRAP (TIR domain-containing adaptor protein). Together, these data suggest that RANKL exposure negatively impacts the macrophage TLR-mediated inflammatory response to bacteria.","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 5","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13198865/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148019770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Neuroimmune Connectome: Understanding how the Peripheral Nervous System shapes Immunity. 神经免疫连接组：了解周围神经系统如何塑造免疫。

ImmunoHorizons Pub Date : 2026-04-22 DOI: 10.1093/immhor/vlaf080

Shanel M Tsuda, Anna-Maria Globig

引用次数: 0

The adaptive immune receptors in a big data world. 大数据世界中的适应性免疫受体。

ImmunoHorizons Pub Date : 2026-04-22 DOI: 10.1093/immhor/vlaf081

Brandon J DeKosky

引用次数: 0

Living rent free in your head: resident memory T cells. 免费居住在你的大脑里：常驻记忆T细胞。

ImmunoHorizons Pub Date : 2026-04-22 DOI: 10.1093/immhor/vlaf074

Hanna N Degefu, Sierra A Kleist, Pamela C Rosato

引用次数: 0

Spatial instruction of tissue immunity. 组织免疫的空间指令。

ImmunoHorizons Pub Date : 2026-04-22 DOI: 10.1093/immhor/vlaf082

Miguel Reina-Campos

{"title":"Spatial instruction of tissue immunity.","authors":"Miguel Reina-Campos","doi":"10.1093/immhor/vlaf082","DOIUrl":"10.1093/immhor/vlaf082","url":null,"abstract":"Tissue immunity must meet the architectural and physiological demands of each organ, from viral entry in the respiratory tract to immune surveillance in the gastrointestinal mucosa. Recent advances in spatial technologies and computational biology now allow us to map entire immune communities in situ, capturing not only their composition but their positional logic, connectivity patterns, and local transcriptional landscapes. These tools are revealing that immune function is not evenly distributed but is patterned along regionalized cytokine gradients, anatomical landmarks, and physical niches that confer specialized capabilities. Understanding the principles driving this spatiotemporal logic is essential to decipher how immune networks are built, maintained, and subverted in disease. To this end, network topology analyses, immune allocation plots, and spatial reference frameworks are beginning to define the \"wiring diagrams\" of immunity, while emerging perturbation-coupled spatial approaches enable causal dissection of the signals that program location-specific phenotypes. These insights have broad implications, from explaining why certain organs resist tumor initiation or metastasis, to revealing metabolic constraints on immune cells in solid tumors, to understanding clonal lymphocyte dynamics in health and disease. Here, we synthesize recent conceptual and technological advances that are transforming how we study tissue immunity; highlight exemplar findings from infection, cancer, and autoimmunity; and outline the experimental and computational innovations needed to bridge key knowledge gaps. We propose that the next phase of immunology will require integrating multiomic, high-resolution spatial data with predictive models of immune behavior to forecast disease risk, design personalized therapies, and ultimately deploy immune protection at the right place and time.","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 S4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13168768/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nasal humoral immunity: the first line of protection against respiratory pathogens. 鼻腔体液免疫：抵御呼吸道病原体的第一道防线。

ImmunoHorizons Pub Date : 2026-04-22 DOI: 10.1093/immhor/vlaf076

Lena Hansen, Jenna J Guthmiller

引用次数: 0

ASPIRE to new horizons. 向往新的视野。

ImmunoHorizons Pub Date : 2026-04-22 DOI: 10.1093/immhor/vlag009

Bonnie N Dittel

引用次数: 0