Journal of Innate Immunity最新文献_第4页

The Roles of Innate Immune Cells in Atopic Dermatitis. 先天性免疫细胞在特应性皮炎中的作用。

IF 4.7 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-07-18 DOI: 10.1159/000539534

Yuke Pan, Youyi Wang, Meinian Xu, Meizhen Zhong, Xiaoming Peng, Kang Zeng, Xiaowen Huang

引用次数: 0

Human Host Defense Peptide LL-37 Suppresses TNFα-Mediated Matrix Metalloproteinases MMP9 and MMP13 in Human Bronchial Epithelial Cells. 人类宿主防御肽 LL-37 可抑制 TNFα 介导的人类支气管上皮细胞基质金属蛋白酶 MMP9 和 MMP13。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-03-12 DOI: 10.1159/000537775

Anthony Altieri, Courtney Lynn Marshall, Padmanie Ramotar, Dylan Lloyd, Mahadevappa Hemshekhar, Victor Spicer, Anne M van der Does, Neeloffer Mookherjee

{"title":"Human Host Defense Peptide LL-37 Suppresses TNFα-Mediated Matrix Metalloproteinases MMP9 and MMP13 in Human Bronchial Epithelial Cells.","authors":"Anthony Altieri, Courtney Lynn Marshall, Padmanie Ramotar, Dylan Lloyd, Mahadevappa Hemshekhar, Victor Spicer, Anne M van der Does, Neeloffer Mookherjee","doi":"10.1159/000537775","DOIUrl":"10.1159/000537775","url":null,"abstract":"Introduction: TNFα-inducible matrix metalloproteinases play a critical role in the process of airway remodeling in respiratory inflammatory disease including asthma. The cationic host defense peptide LL-37 is elevated in the lungs during airway inflammation. However, the impact of LL-37 on TNFα-driven processes is not well understood. Here, we examined the effect of LL-37 on TNFα-mediated responses in human bronchial epithelial cells (HBECs).Methods: We used a slow off-rate modified aptamer-based proteomics approach to define the HBEC proteome altered in response to TNFα. Abundance of selected protein candidates and signaling intermediates was examined using immunoassays, ELISA and Western blots, and mRNA abundance was examined by qRT-PCR.Results: Proteomics analysis revealed that 124 proteins were significantly altered, 12 proteins were enhanced by ≥2-fold compared to unstimulated cells, in response to TNFα. MMP9 was the topmost increased protein in response to TNFα, enhanced by ∼10-fold, and MMP13 was increased by ∼3-fold, compared to unstimulated cells. Furthermore, we demonstrated that LL-37 significantly suppressed TNFα-mediated MMP9 and MMP13 in HBEC. Mechanistic data revealed that TNFα-mediated MMP9 and MMP13 production is controlled by SRC kinase and that LL-37 enhances related upstream negative regulators, namely, phospho-AKT (T308) and TNFα-mediated TNFAIP3 or A20.Conclusions: The findings of this study suggest that LL-37 may play a role in intervening in the process of airway remodeling in chronic inflammatory respiratory disease such as asthma.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"203-215"},"PeriodicalIF":5.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10997319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140110421","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

C4b-Binding Protein and Factor H Attenuate NLRP3 Inflammasome-Mediated Signalling Response during Group A Streptococci Infection in Human Cells. C4b 结合蛋白和因子 H 可抑制 A 组链球菌感染人体细胞时炎症小体的激活。

IF 4.7 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-11-04 DOI: 10.1159/000542434

Serena Bettoni, Mateusz Dziedzic, Damien Bierschenk, Maja Chrobak, Michal Magda, Maisem Laabei, Ben C King, Kristian Riesbeck, Anna M Blom

{"title":"C4b-Binding Protein and Factor H Attenuate NLRP3 Inflammasome-Mediated Signalling Response during Group A Streptococci Infection in Human Cells.","authors":"Serena Bettoni, Mateusz Dziedzic, Damien Bierschenk, Maja Chrobak, Michal Magda, Maisem Laabei, Ben C King, Kristian Riesbeck, Anna M Blom","doi":"10.1159/000542434","DOIUrl":"10.1159/000542434","url":null,"abstract":"Introduction: Streptococcus pyogenes (group A streptococcus; GAS) is a pathogen causing over half a million deaths annually worldwide. Human immune cells respond to GAS infection by activating the NLRP3 inflammasome leading to the release of pro-inflammatory cytokines that control infection. We investigated the role of C4b-binding protein (C4BP) and factor H (FH) in the inflammasome response to GAS, as they are recruited by GAS to prevent complement deposition and limit phagocytosis.Methods: The inflammasome response was investigated using primary human cells and the strain GAS-AP1. Cytokine responses were evaluated by ELISA. C4BP internalisation was investigated using confocal microscopy. Activation of the NLRP3 inflammasome components was assessed by Western blotting.Results: Interleukin-1β (IL-1β) release, induced by GAS-AP1, was inhibited by FH which interferes with priming of human cells. In contrast, C4BP restricted the IL-1β response without affecting cell priming. C4BP was engulfed by cells together with bacteria and excluded from low-pH vesicles but localised within the cytosol and near the ASC speck inflammasome complex. C4BP did not inhibit either the inflammasome complex assembly or caspase-1 activation. However, C4BP limited the cleavage of gasdermin D N-terminal fragments by interfering with caspase-1 enzymatic activity.Conclusion: Given that the amount of IL-1β modulates the severity of GAS infection, our results provide new insights into the effect of FH and internalised C4BP to control GAS sensing by inflammasomes.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"554-572"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637495/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142576341","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

The RNA from Pseudomonas aeruginosa Reduces Neutrophil Responses Favoring Bacterial Survival. 铜绿假单胞菌的 RNA 可降低中性粒细胞的反应，有利于细菌存活。

IF 4.7 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-09-18 DOI: 10.1159/000541414

Jose R Pittaluga, Federico Birnberg-Weiss, Agustina Serafino, Joselyn E Castro, Luis A Castillo, Daiana Martire-Greco, Paula Barrionuevo, Gabriela C Fernández, Verónica I Landoni

{"title":"The RNA from Pseudomonas aeruginosa Reduces Neutrophil Responses Favoring Bacterial Survival.","authors":"Jose R Pittaluga, Federico Birnberg-Weiss, Agustina Serafino, Joselyn E Castro, Luis A Castillo, Daiana Martire-Greco, Paula Barrionuevo, Gabriela C Fernández, Verónica I Landoni","doi":"10.1159/000541414","DOIUrl":"10.1159/000541414","url":null,"abstract":"Introduction: Epithelial and endothelial cells modulate innate immune responses in the lung, including the arrival of neutrophils (PMN), which are crucial cells for the antibacterial host defense. Cells are exposed to prokaryotic RNA (pRNA) during bacterial infections and different pRNA may promote or attenuate the inflammatory response on different immune cells. Pseudomonas aeruginosa (PAE) can cause severe pneumonia and has several immune-evading mechanisms. The aim of this study was to determine the effects of the RNA from PAE (RNAPAE) on lung epithelial, endothelial cells, and PMN, and its impact on bacterial elimination.Methods: Purified total RNAPAE was used as a stimulus on a human lung epithelial cell line (Calu-6), human microvascular endothelial cell line HMEC-1 and isolated healthy human PMN. Activation and cytokine secretion were evaluated. In addition, PMN elimination of live ECO or PAE was determined in the presence of RNAPAE.Results: We found that RNAPAE either induced a pro-inflammatory response on Calu-6 and HMEC-1 or PMN. Pre-stimulation of PMN with RNAPAE diminished activation and chemotaxis induced by live bacteria. Moreover, we found that RNAPAE reduced phagocytosis of live ECO. Finally, we also found that non-degraded fragments of small RNA (<200 bp) were responsible for the PMN microbicidal attenuation during PAE elimination.Conclusion: Our results indicated that short fragments of RNAPAE diminished the immune response of PMN favoring bacterial survival.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"489-500"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11521516/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289292","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

Mechanisms and Therapeutic Strategies for MAFLD Targeting TLR4 Signaling Pathways. 针对 TLR4 信号通路的 MAFLD 机制和治疗策略。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2023-12-21 DOI: 10.1159/000535524

Guanghui Ren, Changchuan Bai, Sitong Yi, Qingwei Cong, Ying Zhu

{"title":"Mechanisms and Therapeutic Strategies for MAFLD Targeting TLR4 Signaling Pathways.","authors":"Guanghui Ren, Changchuan Bai, Sitong Yi, Qingwei Cong, Ying Zhu","doi":"10.1159/000535524","DOIUrl":"10.1159/000535524","url":null,"abstract":"Background: Metabolic-associated fatty liver disease (MAFLD) is one of the most common chronic liver diseases. The underlying pathophysiological mechanisms are intricate and involve various factors. Unfortunately, there is currently a lack of available effective treatment options. Toll-like receptors (TLRs) are a group of pattern-recognition receptors that are responsible for activating the innate immune system. Research has demonstrated that TLR4 plays a pivotal role in the progression of MAFLD by facilitating the pathophysiological mechanisms.Summary: Lipid peroxidation, pro-inflammatory factors, insulin resistance (IR), and dysbiosis of intestinal microbiota are considered as the pathogenic mechanisms of MAFLD. This review summarizes the impact of TLR4 signaling pathways on the progression of MAFLD, specifically in relation to lipid metabolic disorders, IR, oxidative stress, and gut microbiota disorders. Additionally, we emphasize the potential therapeutic approaches for MAFLD that target TLR4 signaling pathways, including the use of plant extracts, traditional Chinese medicines, probiotics, pharmaceuticals such as peroxisome proliferator-activated receptor antagonists and farnesol X agonists, and lifestyle modifications such as dietary changes and exercise also considered. Furthermore, TLR4 signaling pathways have also been linked to the lean MAFLD.Key messages: TLR4 plays a crucial role in MAFLD by triggering IR, buildup of lipids, imbalance in gut microbiota, oxidative stress, and initiation of immune responses. The mitigation of MAFLD can be accomplished by suppressing the TLR4 signaling pathway. In the future, it could potentially emerge as a therapeutic target for the condition.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"45-55"},"PeriodicalIF":5.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10783892/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138830134","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

Metabolism Shapes Immune Responses to Staphylococcus aureus. 代谢影响对金黄色葡萄球菌的免疫反应。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2023-11-28 DOI: 10.1159/000535482

Prabhakar Arumugam, Tammy Kielian

{"title":"Metabolism Shapes Immune Responses to Staphylococcus aureus.","authors":"Prabhakar Arumugam, Tammy Kielian","doi":"10.1159/000535482","DOIUrl":"10.1159/000535482","url":null,"abstract":"Background: Staphylococcus aureus (S. aureus) is a common cause of hospital- and community-acquired infections that can result in various clinical manifestations ranging from mild to severe disease. The bacterium utilizes different combinations of virulence factors and biofilm formation to establish a successful infection, and the emergence of methicillin- and vancomycin-resistant strains introduces additional challenges for infection management and treatment.Summary: Metabolic programming of immune cells regulates the balance of energy requirements for activation and dictates pro- versus anti-inflammatory function. Recent investigations into metabolic adaptations of leukocytes and S. aureus during infection indicate that metabolic crosstalk plays a crucial role in pathogenesis. Furthermore, S. aureus can modify its metabolic profile to fit an array of niches for commensal or invasive growth.Key messages: Here we focus on the current understanding of immunometabolism during S. aureus infection and explore how metabolic crosstalk between the host and S. aureus influences disease outcome. We also discuss how key metabolic pathways influence leukocyte responses to other bacterial pathogens when information for S. aureus is not available. A better understanding of how S. aureus and leukocytes adapt their metabolic profiles in distinct tissue niches may reveal novel therapeutic targets to prevent or control invasive infections.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"12-30"},"PeriodicalIF":5.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10766399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138451589","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

Immunometabolites Direct the Pathogenesis of Bacterial Infection. 免疫代谢物引导着细菌感染的发病机制。

IF 4.7 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-07-01 DOI: 10.1159/000540093

Alice Prince

引用次数: 0

Impact of Extreme Prematurity, Chorioamnionitis, and Sepsis on Neonatal Monocyte Characteristics and Functions. 极度早产、绒毛膜羊膜炎和败血症对新生儿单核细胞特征和功能的影响。

IF 4.7 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-09-14 DOI: 10.1159/000541468

Khaleda Rahman Qazi, Dhanapal Govindaraj, Magalí Martí, Ymke de Jong, Georg Bach Jensen, Thomas Abrahamsson, Maria C Jenmalm, Eva Sverremark-Ekström

{"title":"Impact of Extreme Prematurity, Chorioamnionitis, and Sepsis on Neonatal Monocyte Characteristics and Functions.","authors":"Khaleda Rahman Qazi, Dhanapal Govindaraj, Magalí Martí, Ymke de Jong, Georg Bach Jensen, Thomas Abrahamsson, Maria C Jenmalm, Eva Sverremark-Ekström","doi":"10.1159/000541468","DOIUrl":"10.1159/000541468","url":null,"abstract":"Introduction: The innate branch of the immune system is important in early life, in particular for infants born preterm.Methods: We performed a longitudinal analysis of the peripheral monocyte compartment in extremely preterm children from a randomized, placebo-controlled study of probiotic supplementation. PBMCs and fecal samples were collected at several timepoints during the first months of life. Monocyte characteristics were analyzed by flow cytometry, and LPS-stimulated PBMC culture supernatants were analyzed by Luminex or ELISA. Plasma cytokines and gut microbiota composition were analyzed by ELISA and 16S rRNA-sequencing, respectively.Results: The extremely preterm infants had persistent alterations in their monocyte characteristics that were further aggravated in chorioamnionitis cases. They showed a markedly reduced TLR4 expression and hampered LPS-stimulated cytokine responses 14 days after birth. Notably, at later timepoints, TLR4 expression and LPS responses no longer correlated. Sepsis during the first weeks of life strongly associated with increased pro-inflammatory, and reduced IL-10, responses also at postmenstrual week 36. Further, we report a correlation between gut microbiota features and monocyte phenotype and responses, but also that probiotic supplementation associated with distinct monocyte phenotypic characteristics, without significantly influencing their responsiveness.Conclusion: Extremely preterm infants have monocyte characteristics and functional features that deviate from infants born full-term. Some of these differences persist until they reach an age corresponding to full-term, potentially making them more vulnerable to microbial exposures during the first months of life.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"470-488"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11521501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289291","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

Murine Ribonuclease 6 Limits Bacterial Dissemination during Experimental Urinary Tract Infection. 小鼠核糖核酸酶 6 限制了实验性尿路感染过程中的细菌扩散

IF 4.7 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-05-14 DOI: 10.1159/000539177

Hanna Cortado, Macie Kercsmar, Birong Li, Gabriela Vasquez-Martinez, Sudipti Gupta, Christina Ching, Gregory Ballash, Israel Cotzomi-Ortega, Yuriko I Sanchez-Zamora, Ester Boix, Diana Zepeda-Orozco, Ashley R Jackson, John David Spencer, Juan de Dios Ruiz-Rosado, Brian Becknell

{"title":"Murine Ribonuclease 6 Limits Bacterial Dissemination during Experimental Urinary Tract Infection.","authors":"Hanna Cortado, Macie Kercsmar, Birong Li, Gabriela Vasquez-Martinez, Sudipti Gupta, Christina Ching, Gregory Ballash, Israel Cotzomi-Ortega, Yuriko I Sanchez-Zamora, Ester Boix, Diana Zepeda-Orozco, Ashley R Jackson, John David Spencer, Juan de Dios Ruiz-Rosado, Brian Becknell","doi":"10.1159/000539177","DOIUrl":"10.1159/000539177","url":null,"abstract":"Introduction: The ribonuclease (RNase) A superfamily encodes cationic antimicrobial proteins with potent microbicidal activity toward uropathogenic bacteria. Ribonuclease 6 (RNase6) is an evolutionarily conserved, leukocyte-derived antimicrobial peptide with potent microbicidal activity toward uropathogenic Escherichia coli (UPEC), the most common cause of bacterial urinary tract infections (UTIs). In this study, we generated Rnase6-deficient mice to investigate the hypothesis that endogenous RNase 6 limits host susceptibility to UTI.Methods: We generated a Rnase6EGFP knock-in allele to identify cellular sources of Rnase6 and determine the consequences of homozygous Rnase6 deletion on antimicrobial activity and UTI susceptibility.Results: We identified monocytes and macrophages as the primary cellular sources of Rnase6 in bladders and kidneys of Rnase6EGFP/+ mice. Rnase6 deficiency (i.e., Rnase6EGFP/EGFP) resulted in increased upper urinary tract UPEC burden during experimental UTI, compared to Rnase6+/+ controls. UPEC displayed increased intracellular survival in Rnase6-deficient macrophages.Conclusion: Our findings establish that RNase6 prevents pyelonephritis by promoting intracellular UPEC killing in monocytes and macrophages and reinforce the overarching contributions of endogenous antimicrobial RNase A proteins to host UTI defense.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"283-294"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11250601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140922428","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

Pattern-Recognition Receptors and Immunometabolic Reprogramming: What We Know and What to Explore. 模式识别受体与免疫代谢重编程：我们的认知与探索。

IF 4.7 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-05-13 DOI: 10.1159/000539278

Vijay Kumar, John H Stewart Iv

{"title":"Pattern-Recognition Receptors and Immunometabolic Reprogramming: What We Know and What to Explore.","authors":"Vijay Kumar, John H Stewart Iv","doi":"10.1159/000539278","DOIUrl":"10.1159/000539278","url":null,"abstract":"Background: Evolutionarily, immune response is a complex mechanism that protects the host from internal and external threats. Pattern-recognition receptors (PRRs) recognize MAMPs, PAMPs, and DAMPs to initiate a protective pro-inflammatory immune response. PRRs are expressed on the cell membranes by TLR1, 2, 4, and 6 and in the cytosolic organelles by TLR3, 7, 8, and 9, NLRs, ALRs, and cGLRs. We know their downstream signaling pathways controlling immunoregulatory and pro-inflammatory immune response. However, the impact of PRRs on metabolic control of immune cells to control their pro- and anti-inflammatory activity has not been discussed extensively.Summary: Immune cell metabolism or immunometabolism critically determines immune cells' pro-inflammatory phenotype and function. The current article discusses immunometabolic reprogramming (IR) upon activation of different PRRs, such as TLRs, NLRs, cGLRs, and RLRs. The duration and type of PRR activated, species studied, and location of immune cells to specific organ are critical factors to determine the IR-induced immune response.Key message: The work herein describes IR upon TLR, NLR, cGLR, and RLR activation. Understanding IR upon activating different PRRs is critical for designing better immune cell-specific immunotherapeutics and immunomodulators targeting inflammation and inflammatory diseases.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"295-323"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11250681/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140916636","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