Immunology最新文献

{"title":"Prophylactic Peanut Allergen Ara h 6 Sublingual Immunotherapy Drives Expansion of FoxP3\u0000 +Helios− Regulatory T Cells in the Absence of Allergen-Specific IgA","authors":"Jeppe Madura Larsen,&nbsp;Emma Alberte Lundsgaard,&nbsp;Niels Banhos Danneskiold-Samsøe,&nbsp;Si Brask Sonne,&nbsp;Neil Marcus Rigby,&nbsp;Alan Robert Mackie,&nbsp;Karsten Kristiansen,&nbsp;Katrine Lindholm Bøgh","doi":"10.1111/imm.13883","DOIUrl":"10.1111/imm.13883","url":null,"abstract":"<p>Insights into the underlying immunological mechanisms of prophylactic sublingual immunotherapy (SLIT) may support the development of new strategies for improved prevention and treatment of food allergy. Here, we investigated the humoral, regulatory and sublingual tissue immune response to prophylactic SLIT administration of a single purified peanut allergen in Brown Norway (BN) rats. BN rats received daily sublingual administration of peanut allergen Ara h 6 for three weeks. Suppression of sensitisation was evaluated by subsequent intraperitoneal administration of Ara h 6. Ara h 6-specific IgE, IgA, IgG1 and IgG2a-c levels were measured in serum. The frequency of regulatory T (Treg) cells was analysed using flow cytometry. The sublingual tissue response to Ara h 6 was analysed by transcriptional profiling using mRNA-sequencing. Ara h 6 SLIT protected rats from subsequent sensitisation without inducing a detectable humoral immune response (Ara h 6-specific IgE, IgA, IgG1 and IgG2a-c) in serum. SLIT furthermore promoted the relative expansion of induced Helios⁻ Treg cells within the conventional CD4⁺CD25⁺FoxP3⁺ Treg population in sublingual draining lymph nodes and blood. In conclusion, prophylactic Ara h 6 SLIT drives the relative expansion of induced Helios⁻ Treg cells in the absence of Ara h 6-specific IgA highlighting a potential novel IgA-independent Treg-related immune response at the sublingual mucosal site.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"174 3","pages":"340-348"},"PeriodicalIF":4.9,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13883","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142948217","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}

{"title":"Integration of Immune Responses and Transcriptomic Signatures Reveals the Efficacy of Maternal Genetic Vaccination in a Pregnant Model and Its Neonates","authors":"Sohail Ahmed,&nbsp;Guiqiong Liu,&nbsp;Amber Sadiq,&nbsp;Umar Farooq,&nbsp;Huiguo Yang,&nbsp;Liu Yongbin,&nbsp;Sha Yiyu,&nbsp;Wang Xiaodong,&nbsp;Xunping Jiang","doi":"10.1111/imm.13880","DOIUrl":"https://doi.org/10.1111/imm.13880","url":null,"abstract":"<div>\u0000 \u0000 <p>Maternal vaccination is essential for safeguarding both mother and foetus from infectious diseases. This study investigated the immunogenicity and efficacy of a maternal ORF-<i>B2L</i> genetic vaccine in a pregnant rat model, focusing on maternal–neonatal immune modulation, placental and neonatal spleen transcriptomics and the underlying mechanisms contributing to neonatal immune development. Female rats received intramuscular injections of either a gene vaccine (GV) containing 200 μg of recombinant ORF-<i>B2L</i> DNA and 50 μg of a subunit protein or an empty plasmid as a control. Results showed significantly higher levels of specific anti-<i>B2L</i> antibodies and Th1 and Th2 cytokine levels in both maternal and neonatal sera from the GV group compared to the control group (<i>p</i> &lt; 0.05). Transcriptome analysis identified 1295 differentially expressed genes (DEGs) in the placenta and 998 DEGs in the neonatal spleen, with upregulated pathways associated with immune cell recruitment, cytokine signalling and hormone regulation in the GV group. Notably, upregulated DEGs such as <i>TLR4</i>, <i>ESR1</i> and various cytokine/chemokine-related genes in the placenta suggest enhanced immune regulation and foetal protection. In the neonatal spleen, increased expression of <i>IL-1β</i>, <i>IL-6</i>, <i>IL-10</i> and <i>CD69</i> indicates enhanced T and B cell development and pathogen defence. The upregulation of <i>IL-1β</i> suggests a Th1 response, while elevated <i>IL-10</i> indicates a potential Th2-biased immunity, reflecting a balanced Th1/Th2 response that is crucial for effective adaptive immunity. Overall, maternal ORF-<i>B2L</i> genetic vaccination induces a robust immune response, enhancing maternal-foetal protection and shaping neonatal immune responses, offering valuable insights for optimizing maternal vaccination strategies.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"174 3","pages":"322-339"},"PeriodicalIF":4.9,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143186484","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}

{"title":"Newly Found Rat CD103\u0000 − Dendritic Cells Represent a Highly Immunogenic Subpopulation of Type-2 Conventional Dendritic Cells, Corresponding to Known Dendritic Cell Subsets in Mice and Humans","authors":"Yasushi Sawanobori,&nbsp;Tadayuki Ogawa,&nbsp;Hisashi Ueta,&nbsp;Yusuke Kitazawa,&nbsp;Nobuko Tokuda","doi":"10.1111/imm.13893","DOIUrl":"10.1111/imm.13893","url":null,"abstract":"<div>\u0000 \u0000 <p>Dendritic cells (DCs), the primary antigen-presenting cells, have traditionally been identified by CD103 molecules in rats, whereas mouse and human DCs are identified by CD11c molecules. However, this history does not preclude the existence of CD103⁻ DCs in rats. To explore this possibility, we examined MHCII⁺ cells in rat spleen and thymus, identifying a novel population of CD103⁻MHCII⁺CD45R⁻CD172a⁺ cells. These cells are negative for CD103 and B cell marker CD45R, but positive for the type-2 conventional DC (cDC2) marker CD172a. Transcriptomic analyses revealed that they represent a subpopulation of cDC2. Additionally, gene set enrichment analysis predicted enhanced immunogenic activities for this novel population compared to known rat cDC2s. Mixed leukocyte reaction assays confirmed that the rat CD103⁻ cDC2s induce T cell proliferation more effectively than other DC subsets, suggesting enhanced immunogenic potential. In reaggregated thymic organ culture assays, both the rat CD103⁻ and CD103⁺ cDC2 subsets suppressed the total number of generated thymocytes and skewed the differentiation toward CD8 single-positive cells. Comparisons with previously published single-cell RNA-sequencing datasets showed that the rat CD103⁻ cDC2 subset shares markers and GO terms of known mouse and human cDC2 subpopulations: cDC2a, cDC2b, inf-cDC2, and moDC. In contrast, the classic rat CD103⁺ cDC2 subset expresses only cDC2a markers. These findings provide new insights into DC subpopulations, particularly in species other than mice and humans, where much remains to be uncovered.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"174 4","pages":"384-401"},"PeriodicalIF":4.9,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926999","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}

{"title":"Co-Expression of Dominant-Negative TGF-β Receptor 2 Enhances the Therapeutic Efficacy of Novel TREM1/DAP12-BB-Based CAR-T Cells in Solid Tumours","authors":"Sichao Zhu,&nbsp;Jianping Hu,&nbsp;Jie Lin,&nbsp;Chen Wang,&nbsp;Enxiu Wang","doi":"10.1111/imm.13888","DOIUrl":"10.1111/imm.13888","url":null,"abstract":"<div>\u0000 \u0000 <p>Chimeric antigen receptor (CAR) T-cell therapy has exhibited remarkable efficacy in the treatment of haematological malignancies, yet its application in solid tumours is hindered by the immunosuppressive tumour microenvironment (TME). In this study, a novel SS1-TREM1/DAP12-BB CAR-T cell was devised to target ovarian cancer and further engineered to co-express the dominant-negative TGF-β receptor 2 (DNR) to combat CAR-T cell exhaustion in TME. The incorporation of DNR effectively blocked TGF-β signalling, thereby enhancing CAR-T cell survival and antitumor activity in a TGF-β1-rich environment. In vivo evaluations demonstrated that DNR co-expression potentiated the antitumor efficacy of TREM1/DAP12-BB CAR-T cells and conferred resilience against tumour rechallenge. These findings underscore the broad potential of DNR co-expression in CAR design, presenting a novel therapeutic strategy for patients with recurrent ovarian cancer.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"174 3","pages":"310-321"},"PeriodicalIF":4.9,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921578","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}

{"title":"Interactions of NK Cells and Macrophages: From Infections to Cancer Therapeutics","authors":"Vishakha Hooda,&nbsp;Alpana Sharma","doi":"10.1111/imm.13886","DOIUrl":"10.1111/imm.13886","url":null,"abstract":"<p>The interaction between immune cells brings a consequence either on their role and functioning or the functioning of the other immune cells, modulating the whole mechanistic pathway. The interaction between natural killer (NK) cells and macrophages is one such interaction which is relatively less explored amongst diseased conditions. Their significance comes from their innate nature and secretion of large proportions of cytokines and chemokines which results in influencing adaptive immune responses. Their interplay can lead to several functional outcomes such as NK cell activation/inhibition, increased cytotoxicity and IFNγ release by NK cells, inhibition of macrophage function, etc. This paper delves into the interaction amongst NK cells and macrophages via different receptor-ligands and cytokines, particularly emphasising microbial infections and tumours. The review has the potential to uncover new insights and approaches that could lead to the development of innovative therapeutic tools and targets.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"174 3","pages":"287-295"},"PeriodicalIF":4.9,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13886","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909536","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}

{"title":"FOXP3 Transcriptionally Activates Fatty Acid Scavenger Receptor CD36 in Tumour-Induced Treg Cells","authors":"Subhanki Dhar,&nbsp;Tania Sarkar,&nbsp;Sayantan Bose,&nbsp;Subhadip Pati,&nbsp;Dwaipayan Chakraborty,&nbsp;Dia Roy,&nbsp;Abir K. Panda,&nbsp;Aharna Guin,&nbsp;Sumon Mukherjee,&nbsp;Kuladip Jana,&nbsp;Diptendra K. Sarkar,&nbsp;Gaurisankar Sa","doi":"10.1111/imm.13887","DOIUrl":"10.1111/imm.13887","url":null,"abstract":"<div>\u0000 \u0000 <p>The host immune system is adapted in a variety of ways by tumour microenvironment and growing tumour interacts to promote immune escape. One of these adaptations is manipulating the metabolic processes of cells in the tumour microenvironment. The growing tumour aggressively utilise glucose, its primary energy source available in tumour site, and produce lactate by Warburg effect. In such a hostile environment, tumour-infiltrating immune cells are unable to survive metabolically. Tumour-infiltrating CD4⁺ Treg cells, on the other hand, adapted to an alternative energy-generating system, switching from the highly-competitive glucose to the fatty-acid metabolic pathway, by down-regulating glucose-metabolising genes and up-regulating fatty-acid metabolising genes. Tregs with high-levels of the fatty acid scavenger receptor CD36, a key component of the fatty-acid metabolic pathway, aided this metabolic shift. Treg cell formation was hampered when the fatty-acid metabolic pathway was disrupted, showing that it is necessary for Treg cell development. FOXP3, the Treg lineage-specific transcription factor, regulates fatty-acid metabolism by inducing <i>CD36</i> transcription. A high-fat diet enhanced Treg development while suppressing anti-tumour immunity, whereas a low-fat diet suppressed Treg development. The altered metabolism of tumour-infiltrating Treg cells enables their rapid generation and survival in the hostile tumour microenvironment, aiding cancer progression. Fascinatingly, mice fed with a low-fat diet showed a positive prognosis with chemotherapy than mice fed with a high-fat diet. Thus, a maximum efficacy of chemotherapy might be achieved by altering diet composition during chemotherapy, providing a promising indication for future cancer treatment.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"174 3","pages":"296-309"},"PeriodicalIF":4.9,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907023","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}

{"title":"ITGB4/BNIP3 Activates Autophagy and Reduces MHC-I Expression to Mediate Tumour Immune Escape in Pancreatic Cancer Cell Lines","authors":"Xianfei Zhou,&nbsp;Fan Yang,&nbsp;Luoshun Huang,&nbsp;Yisheng Ling,&nbsp;Renwei Xing,&nbsp;Jie Lu,&nbsp;Hanqiu Nie","doi":"10.1111/imm.13890","DOIUrl":"10.1111/imm.13890","url":null,"abstract":"<div>\u0000 \u0000 <p>This study attempted to identify the relevant pathways involved in autophagy activation of pancreatic cancer and explore the mechanisms underlying immune evasion. Western blot (WB) was used to detect the expression of ITGB4, BNIP3, autophagy-related proteins and MHC-I. Co-immunoprecipitation (Co-IP) was used to verify the binding mode of ITGB4 and BNIP3. Flow cytometry was used to detect the expression of MHC-I on the cell membrane. Transmission electron microscope (TEM) was used to observe cell autophagy. Confocal microscopy was used to observe the co-localisation relationship between MHC-I and autophagosomes in cells. ELISA was used to detect the level of lactate dehydrogenase and granzyme B in a tumour cell-CD8⁺ T-cell co-culture system. Mouse syngeneic transplant tumour model and orthotopic tumour model were constructed and treated with PD-1 monoclonal antibody to observe tumour growth. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the mRNA expression of ITGB4 and BNIP3 in tumour tissues. WB was used to determine the expression of autophagy-related proteins. Flow cytometry was used to detect the expression of MHC-I on cell membranes and the proportion of CD3⁺ and CD8⁺ cells. The results of Co-IP experiments showed that ITGB4 could bind to BNIP3. It was observed under confocal microscopy that activating ITGB4/BNIP3 could promote the phagocytosis of MHC-I by autophagosomes. Finally, the subcutaneous tumour transplantation and orthotopic tumour experiments in mice demonstrated the downregulation of ITGB4 significantly improved the therapeutic effect of PD-1 antibodies on pancreatic cancer. In pancreatic cancer cells, autophagy is positively correlated with the ITGB4-BNIP3 complex protein expression level. Autophagy diminishes the protein expression of MHC-I, thereby promoting immune escape in pancreatic cancer cells.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"174 2","pages":"264-277"},"PeriodicalIF":4.9,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876915","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}

{"title":"Blocking Deoxycytidine Kinase in Activated Lymphocytes Depletes Deoxycytidine Triphosphate Pools and Alters Cell Cycle Kinetics to Yield Less Disease in a Mouse Multiple Sclerosis Model","authors":"Jessica R. Salas,&nbsp;K. M. Ryan,&nbsp;Alyssa O. Trias,&nbsp;Bao Ying Chen,&nbsp;Miriam Guemes,&nbsp;Zoran Galic,&nbsp;Kenneth A. Schultz,&nbsp;Peter M. Clark","doi":"10.1111/imm.13885","DOIUrl":"10.1111/imm.13885","url":null,"abstract":"<div>\u0000 \u0000 <p>Autoreactive, aberrantly activated lymphocytes that target myelin antigens in the central nervous system (CNS) are primary drivers of the autoimmune disease multiple sclerosis (MS). Proliferating cells including activated lymphocytes require deoxyribonucleoside triphosphates (dNTPs) for DNA replication. dNTPs can be synthesised via the de novo pathway from precursors such as glucose and amino acids or the deoxyribonucleoside salvage pathway from extracellular deoxyribonucleosides. Deoxycytidine kinase (dCK) is the rate-limiting enzyme in the salvage pathway. In prior work, we showed that targeting dCK with the small molecule inhibitor TRE-515 limits clinical symptoms in two myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) mouse models of MS and decreases the levels of activated CD4 T and B lymphocytes in vivo. However, whether targeting dCK limits disease in additional EAE models and how targeting dCK directly impacts activated and proliferating CD4 T and B cells has yet to be determined. Here, we show that dCK is activated in the lymph nodes and spleen in an EAE model induced by amino acids 139–151 of the proteolipid protein (PLP_139-151) that is driven by CD4 T and B cells and is characterised by acute disease followed by disease remission. Treating this model with TRE-515 limits clinical symptoms and decreases the levels of activated CD4 T and B cells. In culture, CD4 T and B cells induce deoxyribonucleoside salvage following activation, and TRE-515 directly blocks CD4 T and B cell activation-induced proliferation and activation marker expression. TRE-515 decreases deoxycytidine triphosphate (dCTP) and deoxythymidine triphosphate (dTTP) pools and increases the length of time cells spend in S phase of the cell cycle without inducing a replication stress response in B cells. Our results suggest that dCK activity is required to supply needed dNTPs and to enable rapid cell division following lymphocyte activation against autoantigens in EAE mouse models.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"174 2","pages":"247-263"},"PeriodicalIF":4.9,"publicationDate":"2024-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876941","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}

{"title":"Nucleases: From Primitive Immune Defenders to Modern Biotechnology Tools","authors":"Frank J. Hernandez","doi":"10.1111/imm.13884","DOIUrl":"10.1111/imm.13884","url":null,"abstract":"<p>The story of nucleases begins on the ancient battlefields of early Earth, where simple bacteria fought to survive against viral invaders. Nucleases are enzymes that degrade nucleic acids, with restriction endonucleases emerging as some of the earliest defenders, cutting foreign DNA to protect their bacteria hosts. However, bacteria sought more than just defence. They evolved the CRISPR-Cas system, an adaptive immune mechanism capable of remembering past invaders. The now-famous Cas9 nuclease, a key player in this system, has been harnessed for genome editing, revolutionising biotechnology. Over time, nucleases evolved from basic viral defence tools into complex regulators of immune function in higher organisms. In humans, DNases and RNases maintain immune balance by clearing cellular debris, preventing autoimmunity, and defending against pathogens. These enzymes have transformed from simple bacterial defenders to critical players in both human immunity and biotechnology. This review explores the evolutionary history of nucleases and their vital roles as protectors in the story of life's defence mechanisms.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"174 3","pages":"279-286"},"PeriodicalIF":4.9,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13884","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142835262","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}

{"title":"The Role of Wnt5a in Inflammatory Diseases","authors":"Xin-hua Yu,&nbsp;Xin-ning Guo,&nbsp;Kui Li,&nbsp;Jia-wei Li,&nbsp;Kaijin Wang,&nbsp;Dan Wang,&nbsp;Bi-cui Liu","doi":"10.1111/imm.13882","DOIUrl":"10.1111/imm.13882","url":null,"abstract":"<p>Wnt5a plays an important role in cell development and maturation and is closely associated with various diseases, such as malignant tumours, metabolic disorders, fibrosis, growth and development. Recent studies have shown that Wnt5a expression and signal transduction are strongly involved in the inflammatory response. This study comprehensively reviewed the latest research progress on the association between Wnt5a and several inflammatory diseases, such as sepsis, asthma, chronic obstructive pulmonary disease, tuberculosis, rheumatoid arthritis, atherosclerosis and psoriasis vulgare. We elucidated the mechanism by which the Wnt5a protein is involved in the pathogenesis of these diseases, providing a basis for the prevention and treatment of inflammatory diseases.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"174 2","pages":"203-212"},"PeriodicalIF":4.9,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13882","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817925","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}