Immune Network最新文献_第2页

Erratum: Inhibition of Chitinase-3-like-1 by K284-6111 Reduces Atopic Skin Inflammation via Repressing Lactoferrin. 更正：K284-6111抑制几丁质酶-3-样-1可通过抑制乳铁蛋白减轻特应性皮肤炎症。

IF 4.3 4区医学

Immune Network Pub Date : 2024-05-29 eCollection Date: 2024-06-01 DOI: 10.4110/in.2024.24.e22

Seong Hee Jeon, Yong Sun Lee, In Jun Yeo, Hee Pom Lee, Jaesuk Yoon, Dong Ju Son, Sang-Bae Han, Jin Tae Hong

引用次数: 0

IL-1 Receptor Dynamics in Immune Cells: Orchestrating Immune Precision and Balance. 免疫细胞中的 IL-1 受体动力学：协调免疫精确性和平衡。

IF 4.3 4区医学

Immune Network Pub Date : 2024-05-29 eCollection Date: 2024-06-01 DOI: 10.4110/in.2024.24.e21

Dong Hyun Kim, Won-Woo Lee

{"title":"IL-1 Receptor Dynamics in Immune Cells: Orchestrating Immune Precision and Balance.","authors":"Dong Hyun Kim, Won-Woo Lee","doi":"10.4110/in.2024.24.e21","DOIUrl":"10.4110/in.2024.24.e21","url":null,"abstract":"IL-1, a pleiotropic cytokine with profound effects on various cell types, particularly immune cells, plays a pivotal role in immune responses. The proinflammatory nature of IL-1 necessitates stringent control mechanisms of IL-1-mediated signaling at multiple levels, encompassing transcriptional and translational regulation, precursor processing, as well as the involvement of a receptor accessory protein, a decoy receptor, and a receptor antagonist. In T-cell immunity, IL-1 signaling is crucial during both the priming and effector phases of immune reactions. The fine-tuning of IL-1 signaling hinges upon two distinct receptor types; the functional IL-1 receptor (IL-1R) 1 and the decoy IL-1R2, accompanied by ancillary molecules such as the IL-1R accessory protein (IL-1R3) and IL-1R antagonist. IL-1R1 signaling by IL-1β is critical for the differentiation, expansion, and survival of Th17 cells, essential for defense against extracellular bacteria or fungi, yet implicated in autoimmune disease pathogenesis. Recent investigations emphasize the physiological importance of IL-1R2 expression, particularly in its capacity to modulate IL-1-dependent responses within Tregs. The precise regulation of IL-1R signaling is indispensable for orchestrating appropriate immune responses, as unchecked IL-1 signaling has been implicated in inflammatory disorders, including Th17-mediated autoimmunity. This review provides a thorough exploration of the IL-1R signaling complex and its pivotal roles in immune regulation. Additionally, it highlights recent advancements elucidating the mechanisms governing the expression of IL-1R1 and IL-1R2, underscoring their contributions to fine-tuning IL-1 signaling. Finally, the review briefly touches upon therapeutic strategies targeting IL-1R signaling, with potential clinical applications.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11224669/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141556487","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

The Impact of Pulmonary Disorders on Neurological Health (Lung-Brain Axis). 肺部疾病对神经系统健康的影响（肺-脑轴）。

IF 4.3 4区医学

Immune Network Pub Date : 2024-05-29 eCollection Date: 2024-06-01 DOI: 10.4110/in.2024.24.e20

Hongryeol Park, Chan Hee Lee

引用次数: 0

Influenza Virus-Derived CD8 T Cell Epitopes: Implications for the Development of Universal Influenza Vaccines. 流感病毒衍生的 CD8 T 细胞表位：开发通用流感疫苗的意义。

IF 4.3 4区医学

Immune Network Pub Date : 2024-05-07 eCollection Date: 2024-06-01 DOI: 10.4110/in.2024.24.e19

Sang-Hyun Kim, Erica Españo, Bill Thaddeus Padasas, Ju-Ho Son, Jihee Oh, Richard J Webby, Young-Ran Lee, Chan-Su Park, Jeong-Ki Kim

{"title":"Influenza Virus-Derived CD8 T Cell Epitopes: Implications for the Development of Universal Influenza Vaccines.","authors":"Sang-Hyun Kim, Erica Españo, Bill Thaddeus Padasas, Ju-Ho Son, Jihee Oh, Richard J Webby, Young-Ran Lee, Chan-Su Park, Jeong-Ki Kim","doi":"10.4110/in.2024.24.e19","DOIUrl":"10.4110/in.2024.24.e19","url":null,"abstract":"The influenza virus poses a global health burden. Currently, an annual vaccine is used to reduce influenza virus-associated morbidity and mortality. Most influenza vaccines have been developed to elicit neutralizing Abs against influenza virus. These Abs primarily target immunodominant epitopes derived from hemagglutinin (HA) or neuraminidase (NA) of the influenza virus incorporated in vaccines. However, HA and NA are highly variable proteins that are prone to antigenic changes, which can reduce vaccine efficacy. Therefore, it is essential to develop universal vaccines that target immunodominant epitopes derived from conserved regions of the influenza virus, enabling cross-protection among different virus variants. The internal proteins of the influenza virus serve as ideal targets for universal vaccines. These internal proteins are presented by MHC class I molecules on Ag-presenting cells, such as dendritic cells, and recognized by CD8 T cells, which elicit CD8 T cell responses, reducing the likelihood of disease and influenza viral spread by inducing virus-infected cell apoptosis. In this review, we highlight the importance of CD8 T cell-mediated immunity against influenza viruses and that of viral epitopes for developing CD8 T cell-based influenza vaccines.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11224667/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554660","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

Cytokine Storm Related to CD4⁺ T Cells in Influenza Virus-Associated Acute Necrotizing Encephalopathy. 流感病毒相关急性坏死性脑病中与 CD4+ T 细胞有关的细胞因子风暴

IF 6 4区医学

Immune Network Pub Date : 2024-04-29 eCollection Date: 2024-04-01 DOI: 10.4110/in.2024.24.e18

Shushu Wang, Dongyao Wang, Xuesong Wang, Mingwu Chen, Yanshi Wang, Haoquan Zhou, Yonggang Zhou, Yong Lv, Haiming Wei

{"title":"Cytokine Storm Related to CD4+ T Cells in Influenza Virus-Associated Acute Necrotizing Encephalopathy.","authors":"Shushu Wang, Dongyao Wang, Xuesong Wang, Mingwu Chen, Yanshi Wang, Haoquan Zhou, Yonggang Zhou, Yong Lv, Haiming Wei","doi":"10.4110/in.2024.24.e18","DOIUrl":"10.4110/in.2024.24.e18","url":null,"abstract":"Acute necrotizing encephalopathy (ANE) is a rare but deadly complication with an unclear pathogenesis. We aimed to elucidate the immune characteristics of H1N1 influenza virus-associated ANE (IANE) and provide a potential therapeutic approach for IANE. Seven pediatric cases from a concentrated outbreak of H1N1 influenza were included in this study. The patients' CD4+ T cells from peripheral blood decreased sharply in number but highly expressed Eomesodermin (Eomes), CD69 and PD-1, companied with extremely high levels of IL-6, IL-8 in the cerebrospinal fluid and plasma. Patient 2, who showed high fever and seizures and was admitted to the hospital very early in the disease course, received intravenous tocilizumab and subsequently showed a reduction in temperature and a stable conscious state 24 h later. In conclusion, a proinflammatory cytokine storm associated with activated CD4+ T cells may cause severe brain pathology in IANE. Tocilizumab may be helpful in treating IANE.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11076295/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140898304","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

Decay-Accelerating Factor Differentially Associates With Complement-Mediated Damage in Synovium After Meniscus Tear as Compared to Anterior Cruciate Ligament Injury. 与前十字韧带损伤相比，半月板撕裂后衰变加速因子与补体介导的滑膜损伤有不同的关联。

IF 6 4区医学

Immune Network Pub Date : 2024-04-29 eCollection Date: 2024-04-01 DOI: 10.4110/in.2024.24.e17

V Michael Holers, Rachel M Frank, Michael Zuscik, Carson Keeter, Robert I Scheinman, Christopher Striebich, Dmitri Simberg, Michael R Clay, Larry W Moreland, Nirmal K Banda

{"title":"Decay-Accelerating Factor Differentially Associates With Complement-Mediated Damage in Synovium After Meniscus Tear as Compared to Anterior Cruciate Ligament Injury.","authors":"V Michael Holers, Rachel M Frank, Michael Zuscik, Carson Keeter, Robert I Scheinman, Christopher Striebich, Dmitri Simberg, Michael R Clay, Larry W Moreland, Nirmal K Banda","doi":"10.4110/in.2024.24.e17","DOIUrl":"10.4110/in.2024.24.e17","url":null,"abstract":"We have reported that anterior cruciate ligament (ACL) injury leads to the differential dysregulation of the complement system in the synovium as compared to meniscus tear (MT) and proposed this as a mechanism for a greater post-injury prevalence of post traumatic osteoarthritis (PTOA). To explore additional roles of complement proteins and regulators, we determined the presence of decay-accelerating factor (DAF), C5b, and membrane attack complexes (MACs, C5b-9) in discarded surgical synovial tissue (DSST) collected during arthroscopic ACL reconstructive surgery, MT-related meniscectomy, osteoarthritis (OA)-related knee replacement surgery and normal controls. Multiplexed immunohistochemistry was used to detect and quantify complement proteins. To explore the involvement of body mass index (BMI), after these 2 injuries, we examined correlations among DAF, C5b, MAC and BMI. Using these approaches, we found that synovial cells after ACL injury expressed a significantly lower level of DAF as compared to MT (p<0.049). In contrast, C5b staining synovial cells were significantly higher after ACL injury (p<0.0009) and in OA DSST (p<0.039) compared to MT. Interestingly, there were significantly positive correlations between DAF & C5b (r=0.75, p<0.018) and DAF & C5b (r=0.64 p<0.022) after ACL injury and MT, respectively. The data support that DAF, which should normally dampen C5b deposition due to its regulatory activities on C3/C5 convertases, does not appear to exhibit that function in inflamed synovia following either ACL injury or MT. Ineffective DAF regulation may be an additional mechanism by which relatively uncontrolled complement activation damages tissue in these injury states.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11076301/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140898350","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

Beyond the CAR T Cells: TIL Therapy for Solid Tumors. 超越 CAR T 细胞：治疗实体瘤的 TIL疗法。

IF 6 4区医学

Immune Network Pub Date : 2024-04-18 eCollection Date: 2024-04-01 DOI: 10.4110/in.2024.24.e16

Rohit Singh

引用次数: 0

Oxidized LDL Accelerates Cartilage Destruction and Inflammatory Chondrocyte Death in Osteoarthritis by Disrupting the TFEB-Regulated Autophagy-Lysosome Pathway. 氧化低密度脂蛋白通过干扰 TFEB 调节的自噬-溶酶体途径，加速骨关节炎中软骨的破坏和炎性软骨细胞的死亡

IF 4.3 4区医学

Immune Network Pub Date : 2024-04-12 eCollection Date: 2024-06-01 DOI: 10.4110/in.2024.24.e15

Jeong Su Lee, Yun Hwan Kim, JooYeon Jhun, Hyun Sik Na, In Gyu Um, Jeong Won Choi, Jin Seok Woo, Seung Hyo Kim, Asode Ananthram Shetty, Seok Jung Kim, Mi-La Cho

{"title":"Oxidized LDL Accelerates Cartilage Destruction and Inflammatory Chondrocyte Death in Osteoarthritis by Disrupting the TFEB-Regulated Autophagy-Lysosome Pathway.","authors":"Jeong Su Lee, Yun Hwan Kim, JooYeon Jhun, Hyun Sik Na, In Gyu Um, Jeong Won Choi, Jin Seok Woo, Seung Hyo Kim, Asode Ananthram Shetty, Seok Jung Kim, Mi-La Cho","doi":"10.4110/in.2024.24.e15","DOIUrl":"10.4110/in.2024.24.e15","url":null,"abstract":"Osteoarthritis (OA) involves cartilage degeneration, thereby causing inflammation and pain. Cardiovascular diseases, such as dyslipidemia, are risk factors for OA; however, the mechanism is unclear. We investigated the effect of dyslipidemia on the development of OA. Treatment of cartilage cells with low-density lipoprotein (LDL) enhanced abnormal autophagy but suppressed normal autophagy and reduced the activity of transcription factor EB (TFEB), which is important for the function of lysosomes. Treatment of LDL-exposed chondrocytes with rapamycin, which activates TFEB, restored normal autophagy. Also, LDL enhanced the inflammatory death of chondrocytes, an effect reversed by rapamycin. In an animal model of hyperlipidemia-associated OA, dyslipidemia accelerated the development of OA, an effect reversed by treatment with a statin, an anti-dyslipidemia drug, or rapamycin, which activates TFEB. Dyslipidemia reduced the autophagic flux and induced necroptosis in the cartilage tissue of patients with OA. The levels of triglycerides, LDL, and total cholesterol were increased in patients with OA compared to those without OA. The C-reactive protein level of patients with dyslipidemia was higher than that of those without dyslipidemia after total knee replacement arthroplasty. In conclusion, oxidized LDL, an important risk factor of dyslipidemia, inhibited the activity of TFEB and reduced the autophagic flux, thereby inducing necroptosis in chondrocytes.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11224671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554662","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

Th17 Cell and Inflammatory Infiltrate Interactions in Cutaneous Leishmaniasis: Unraveling Immunopathogenic Mechanisms. 皮肤利什曼病中 Th17 细胞与炎症浸润的相互作用：揭示免疫致病机制

IF 6 4区医学

Immune Network Pub Date : 2024-03-27 eCollection Date: 2024-04-01 DOI: 10.4110/in.2024.24.e14

Abraham U Morales-Primo, Ingeborg Becker, Claudia Patricia Pedraza-Zamora, Jaime Zamora-Chimal

{"title":"Th17 Cell and Inflammatory Infiltrate Interactions in Cutaneous Leishmaniasis: Unraveling Immunopathogenic Mechanisms.","authors":"Abraham U Morales-Primo, Ingeborg Becker, Claudia Patricia Pedraza-Zamora, Jaime Zamora-Chimal","doi":"10.4110/in.2024.24.e14","DOIUrl":"10.4110/in.2024.24.e14","url":null,"abstract":"The inflammatory response during cutaneous leishmaniasis (CL) involves immune and non-immune cell cooperation to contain and eliminate Leishmania parasites. The orchestration of these responses is coordinated primarily by CD4+ T cells; however, the disease outcome depends on the Th cell predominant phenotype. Although Th1 and Th2 phenotypes are the most addressed as steers for the resolution or perpetuation of the disease, Th17 cell activities, especially IL-17 release, are recognized to be vital during CL development. Th17 cells perform vital functions during both acute and chronic phases of CL. Overall, Th17 cells induce the migration of phagocytes (neutrophils, macrophages) to the infection site and CD8+ T cells and NK cell activation. They also provoke granzyme and perforin secretion from CD8+ T cells, macrophage differentiation towards an M2 phenotype, and expansion of B and Treg cells. Likewise, immune cells from the inflammatory infiltrate have modulatory activities over Th17 cells involving their differentiation from naive CD4+ T cells and further expansion by generating a microenvironment rich in optimal cytokines such as IL-1β, TGF-β, IL-6, and IL-21. Th17 cell activities and synergies are crucial for the resistance of the infection during the early and acute stages; however, if unchecked, Th17 cells might lead to a chronic stage. This review discusses the synergies between Th17 cells and the inflammatory infiltrate and how these interactions might destine the course of CL.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11076297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140898360","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

Cytokines and Immune Disorders: Illuminating Cytokines as Hubs Within the Immune Network. 细胞因子与免疫失调：阐明细胞因子在免疫网络中的枢纽作用。

IF 6 4区医学

Immune Network Pub Date : 2024-02-26 eCollection Date: 2024-02-01 DOI: 10.4110/in.2024.24.e13

Seung-Woo Lee, Chong-Kil Lee

引用次数: 0