Scandinavian Journal of Immunology最新文献

{"title":"<scp>IgG</scp> exacerbates genital chlamydial pathology in females by enhancing pathogenic <scp>CD8</scp>⁺ T cell responses","authors":"Charles W. Armitage, Connor P. O'Meara, Emily R. Bryan, Avinash Kollipara, Logan K. Trim, Danica Hickey, Alison J. Carey, Wilhelmina M. Huston, Gavin Donnelly, Anusch Yazdani, Richard S. Blumberg, Kenneth W. Beagley","doi":"10.1111/sji.13331","DOIUrl":"https://doi.org/10.1111/sji.13331","url":null,"abstract":"Abstract Chlamydia trachomatis infections are an important sexually transmitted infection that can lead to inflammation, scarring and hydrosalpinx/infertility. However, infections are commonly clinically asymptomatic and do not receive treatment. The underlying cause of asymptomatic immunopathology remains unknown. Here, we demonstrate that IgG produced during male infection enhanced the incidence of immunopathology and infertility in females. Human endocervical cells expressing the neonatal Fc Receptor (FcRn) increased translocation of human IgG‐opsonized C. trachomatis . Using total IgG purified from infected male mice, we opsonized C. muridarum and then infected female mice, mimicking sexual transmission. Following infection, IgG‐opsonized Chlamydia was found to transcytose the epithelial barrier in the uterus, where it was phagocytosed by antigen‐presenting cells (APCs) and trafficked to the draining lymph nodes. APCs then expanded both CD4 + and CD8 + T cell populations and caused significantly more infertility in female mice infected with non‐opsonized Chlamydia . Enhanced phagocytosis of IgG‐opsonized Chlamydia significantly increased pro‐inflammatory signalling and T cell proliferation. As IgG is transcytosed by FcRn, we utilized FcRn −/− mice and observed that shedding kinetics of Chlamydia were only affected in FcRn −/− mice infected with IgG‐opsonized Chlamydia . Depletion of CD8 + T cells in FcRn −/− mice lead to a significant reduction in the incidence of infertility. Taken together, these data demonstrate that IgG seroconversion during male infection can amplify female immunopathology, dependent on FcRn transcytosis, APC differentiation and enhanced CD8 T cell responses.","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135917847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Were athletes at increased risk of sudden cardiac death and survived sudden cardiac arrest in 2021?","authors":"Søren Roest Korsgaard","doi":"10.1111/sji.13334","DOIUrl":"https://doi.org/10.1111/sji.13334","url":null,"abstract":"In a letter dated December 2022, Polykretis and McCullough reported that there had been an increase in sudden cardiac death (SCD) and survived sudden cardiac arrest (SCA) among athletes from 2021 until the date the letter was submitted.1 In the letter, they cited a database purportedly containing 1598 instances of athletes having experienced SCA or SCA during the mentioned timeframe.2 When I examined the database, however, I did not find support for the claim. A number of the cases in the database were unrelated to elite sports as well as SCD or SCA. For example, in some cases, the stated cause of death was suicide. In a different instance, a 70-year-old man reportedly experienced SCD while cycling. The referenced database was clearly disorganized and did not provide evidence of the stated claim. Whether or not there was an increase in SCD and SCA has been the subject of considerable debate, but as far as I am aware no scientific investigation has been conducted.3 This prompted me to look further. In the letter, Polykretis and McCullough compared the data with a systematic review by Bille, Figueiras, Schamasch, et al, who reported that from 1966 to 2004, a total of 1101 athletes under the age of 35 had died as a result of various heart-related conditions. However, such a broad comparison may not be the best approach for assessing whether athletes were at an increased risk of SCA and SCD in 2021 in comparison with pre-COVID data. I would argue that a more appropriate comparison can be drawn if we exclusively focus on cases of SCA and SCD among elite footballers, as this subject has been extensively studied. As elite footballers are in the media spotlight, cases of SCA and SCD are unlikely to be overlooked. Cases occurring at recreational and competitive levels are less likely to receive significant media coverage or be recorded by surveillance systems. The pre-COVID rate of SCA and SCD among footballers was assessed in a prospective, observational study by Egger et al4 known as the FIFA study. Globally, the study found a total of 617 cases of SCD and SCA from 2014 to 2018. A total of 475 died. The study also included a few cases from related sports, including beach soccer, walking football, and futsal. Out of the 617 cases, a total of 95% occurred at the amateur level, which encompassed both recreational and competitive players. It only found 33 cases classified as elite level, amounting to 6.6 cases per year on average. The study was confined to cases during football-specific exercise, such as during training or a match, or within 1 h after cessation of such activity. In the context of this letter, let x denote the number of cases of SCD and SCA in 2021, that is, 10 cases, and let x! = 1 × 2 × 3 × 4 × … × x. Further, let λ be the average rate, namely 6.6 cases. Euler's constant, e ≈ $$ approx $$ 2.71828. It can easily be shown that the 10 cases are not statistically significant, that is, P X ≥ 10 = 0.131 > 0.05 = α $$ Pleft[Xge 10right]=0.131>0.0","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135146517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"No indication of aberrant neutrophil extracellular trap release in indolent or advanced systemic mastocytosis","authors":"Axel Rosell, Cecilia Karlström, Joakim S. Dahlin, Daryl Boey, Monika Klimkowska, Kajsa Ax, Charlotte Thålin, Johanna Ungerstedt","doi":"10.1111/sji.13333","DOIUrl":"https://doi.org/10.1111/sji.13333","url":null,"abstract":"Abstract In disease states with chronic inflammation, there is a crosstalk between mast cells and neutrophil granulocytes in the inflamed microenvironment, which may be potentiated by tryptase. In systemic mastocytosis (SM), mast cells are constitutively active and tryptase is elevated in blood. Mast cell activation in SM leads to symptoms from various organs depending on where the active mast cells reside, for example, palpitations, flush, allergic symptoms including anaphylactic reactions, and osteoporosis. Whether neutrophil function is altered in SM is not well understood. In the current study, we assessed nucleosomal citrullinated histone H3 (H3Cit‐DNA) as a proxy for neutrophil extracellular trap release in plasma from 55 patients with indolent and advanced SM. We observed a strong trend towards a correlation between leukocyte count, eosinophil count and neutrophil count and H3Cit‐DNA levels in patients with advanced SM but not in indolent SM; however, no differences in H3Cit‐DNA levels in SM patients compared with healthy controls. H3Cit‐DNA levels did not correlate with SM disease burden, tryptase levels, history of anaphylaxis or presence of cutaneous mastocytosis; thus, there is no evidence of a general neutrophil extracellular trap release in SM. Interestingly, H3Cit‐DNA levels and leukocyte counts were elevated in a subgroup of SM patients with aberrant mast cell CD2 expression, which warrants further investigation. In conclusion, we found no evidence of global increase in neutrophil extracellular trap release in SM.","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135250744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aicardi-Goutières syndrome: A monogenic type I interferonopathy.","authors":"Anran Liu, Songcheng Ying","doi":"10.1111/sji.13314","DOIUrl":"10.1111/sji.13314","url":null,"abstract":"<p><p>Aicardi-Goutières syndrome (AGS) is a rare monogenic autoimmune disease that primarily affects the brains of children patients. Its main clinical features include encephalatrophy, basal ganglia calcification, leukoencephalopathy, lymphocytosis and increased interferon-α (IFN-α) levels in the patient's cerebrospinal fluid (CSF) and serum. AGS may be caused by mutations in any one of nine genes (TREX1, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, ADAR1, IFIH1, LSM11 and RNU7-1) that result in accumulation of self-nucleic acids in the cytoplasm or aberrant sensing of self-nucleic acids. This triggers overproduction of type I interferons (IFNs) and subsequently causes AGS, the prototype of type I interferonopathies. This review describes the discovery history of AGS with various genotypes and provides the latest knowledge of clinical manifestations and causative genes of AGS. The relationship between AGS and type I interferonopathy and potential therapeutic methods for AGS are also discussed in this review.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10195710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The prognostic significance of CDK6 expression in renal cell carcinoma treated by immune checkpoint plus tyrosine kinase inhibition.","authors":"Jiajun Wang, Sihong Zhang, Ying Wang, Yanjun Zhu, Xianglai Xu, Jianming Guo","doi":"10.1111/sji.13304","DOIUrl":"10.1111/sji.13304","url":null,"abstract":"<p><p>Checkpoint inhibitor immunotherapy plus tyrosine kinase inhibitor (IO/TKI) has become the first-line treatment for metastatic renal cell carcinoma (RCC), despite the lack of biomarkers. Cyclin-dependent kinase 6 (CDK6) has shown a regulatory role in antitumour response. The study enrolled two cohorts of metastatic RCC treated by IO/TKI (Zhongshan Hospital [ZS]-MRCC, n = 45; JAVELIN-101, n = 726) and two cohorts of localized RCC (ZS-HRRCC, n = 40; TCGA-KIRC, n = 530). CDK6 was evaluated by RNA-sequencing. Progression-free survival (PFS) was the primary endpoint. The prognostic role of CDK6 was evaluated by survival analysis. The correlation between CDK6 and tumour microenvironment was assessed by immunohistochemistry and flow cytometry. The high-CDK6 group displayed a lower response rate (13.6%) than the low-CDK6 group (56.5%) (P = .002). High-CDK6 was associated with poor PFS in both the ZS-MRCC cohort (high-CDK6, median PFS 6.4 months; low-CDK6, median PFS not reached; P = .010) and JAVELIN-101 cohort (high-CDK6, median PFS 10.0 months; low-CDK6, median PFS 13.3 month; P = .033). High-CDK6 was associated with increased PD1⁺ CD8⁺ T cells (Spearman's ρ = .47, P < .001) and decreased Granzyme B⁺ CD8⁺ T cells (Spearman's ρ = -.35, P = .030). Finally, a random forest score (RFscore) was built by integrating CDK6 and immunologic genes, which was associated with survival benefits of IO/TKI (RFscore-low, TKI vs IO/TKI, HR = 2.47, 95% CI 1.82-3.35, P < .001; RFscore-high, TKI vs IO/TKI, HR = 0.99, 95% CI 0.75-1.32, P = .963). Elevated CDK6 expression indicated resistance and poor PFS under IO/TKI therapy, which was related to exhausted CD8⁺ T cells. Integrated RFscore could evaluate the benefits of IO/TKI.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10248724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of BNT162b2 and mRNA1273 vaccines in solid organ transplant recipients: Post-Hoc analysis of a Japanese national prospective study.","authors":"Mikiko Yoshikawa, Yoichiro Natori, Rikako Oki, Kohei Unagami, Satoko Ohfuji, Ryoichi Imamura, Hideki Ishida, Shiro Takahara, Yoshio Hirota, Hiroto Egawa","doi":"10.1111/sji.13308","DOIUrl":"10.1111/sji.13308","url":null,"abstract":"<p><p>The coronavirus disease-19 (COVID-19) vaccine efficacy and immunogenicity in the immunocompetent population are well established. However, in solid organ transplant (SOT) recipients, because of their use of immunosuppressive medication, the immunogenicity of these severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines remains suboptimal. Both BNT162b2 and mRNA1273 have been used for some time, but their immunogenicity has not been directly compared in this immunocompromised patient group. We performed a post-hoc analysis of a previous prospective cohort study. The inclusion criteria were adult SOT recipients with active grafts at least 1 month after SOT. After giving consent, participants chose to receive either BNT162b2 or mRNA1273 vaccine. Anti-spike-protein-S antibody against SARS-CoV-2 was measured. Propensity scores were calculated via logistic regression to transform the probability of having received either BNT162b2 or mRNA1273 vaccine, and a model was developed. We enrolled 623 SOT recipients. In the propensity score-matched analysis, 100 recipients were selected for BNT162b2 and 100 for mRNA1273. SARS-CoV-2 anti-spike protein antibody positivity with BNT162b2 versus mRNA1273 at 3 weeks after the first dose, 1 month after the second dose, 3 months after the second dose, and 6 months after the second dose were 10% versus 19% (P = .07), 51% versus 58% (P = .30), 74% versus 88% (P = .01), and 78% versus 87% (P = .13), respectively. We conducted a propensity score-matched comparison of BNT162b2 and mRNA1273 vaccines as the primary series of COVID-19 vaccines in SOT recipients. We found significantly better immunogenicity with the mRNA1273 vaccine than with BNT162b2.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46105778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of B-1 cell numbers and B cell-mediated antibody production by Inpp4b.","authors":"Meizhen Xu, Jinfeng Ren, Wenyu Jia, Siyu Wang, Yuting Liu, Xinzhu Chen, Jianhong Shi, Hui Wang","doi":"10.1111/sji.13309","DOIUrl":"10.1111/sji.13309","url":null,"abstract":"<p><p>T and B lymphocytes are crucial players in cellular and humoral immune responses. The development, activation and differentiation of T and B lymphocytes are regulated by the best characterized PI3K-PI (3,4,5) P3-AKT phosphoinositide signalling pathway. As a branch of the phosphoinositide signalling pathway, the lipid phosphatase INPP4B inhibits AKT activation through degrading the phosphoinositide signalling messenger PI (3,4) P2. However, the role of Inpp4b in T and B lymphocytes remains elusive. Here, we reported that Inpp4b was highly expressed in human and murine T- and B-1 lymphocytes. Despite its higher expression in T lymphocytes, neither T cell development and homeostasis nor in vitro T cell activation and CD4⁺ T cell differentiation were altered upon loss of Inpp4b. Interestingly, combined direct phenotype analysis of Inpp4b conventional knockout mice and adoptive transfer studies revealed that ablation of Inpp4b intrinsically reduced peritoneal B-1 cells rather B-2 cells. Moreover, Inpp4b deficiency led to impaired thymus independent (TI) and thymus dependent (TD) antigens-induced antibody production. Further in vitro analysis revealed that CD40-mediated B cell proliferation was impaired upon ablation of Inpp4b. Our findings reveal that Inpp4b is required in regulating B-1 cell numbers and B cell-mediated antibody production.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10196632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progress in research on the role played by myeloid-derived suppressor cells in liver diseases.","authors":"Qianqian Sun, Heng Dai, Siliang Wang, Yuanyuan Chen, Huilian Shi","doi":"10.1111/sji.13312","DOIUrl":"10.1111/sji.13312","url":null,"abstract":"<p><p>Myeloid-derived suppressor cells (MDSCs) refer to a group of immature myeloid cells with potent immunosuppressive capacity upon activation by pathological conditions. Because of their potent immunosuppressive ability, MDSCs have garnered extensive attention in the past few years in the fields of oncology, infection, chronic inflammation and autoimmune diseases. Research on MDSCs in liver diseases has gradually increased, and their potential therapeutic roles will be further explored. This review presents a summary of the involvement and the role played by MDSCs in liver diseases, thus identifying their potential targets for the treatment of liver diseases and providing new directions for liver disease-related research.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45424622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aggregation-prone peptides from within a non-self-protein homoaggregate are preferred for MHC association: Historical overview.","authors":"Donald R Forsdyke","doi":"10.1111/sji.13306","DOIUrl":"10.1111/sji.13306","url":null,"abstract":"<p><p>New technologies assist re-evaluation of hypotheses on generation of immune cell repertoires and distinctions of self from non-self. Findings include positive correlations between peptide propensities to aggregate and their binding to major histocompatibility complex (MHC) proteins. This recalls the hypothesis that foreign proteins may homoaggregate in host cytosols prior to releasing their peptides (p) to form pMHC complexes. Clues to this included aggregation-related phenomena associated with infections (rouleaux formation, pyrexia, certain brain diseases). By virtue of 'promiscuous' gene expression by thymic presenting cells - perhaps adapted from earlier evolving gonadal mechanisms - developing T cells monitor surface pMHC clusterings. This evaluates intracellular concentrations of the corresponding proteins, and hence, following Burnet's two signal principle, degrees of self-reactivity. After positive selection in the thymic cortex for reactivity with 'near-self', high-level pMHC clustering suffices in the medulla for negatively selection. Following Burnet's principle, in the periphery low-level clustering suffices for T cell stimulation and high-level clustering again provokes negative selection (immunological tolerance). For evolving intracellular pathogens, fine-tuned polymorphisms of their host species have limited to 'near-self' some mimicking adaptations. It is proposed that while entire pathogen proteins may have evolved to minimize their aggregability, the greater aggregability of their peptides remains partially hidden within. Two-step proofreading mechanisms in prospective hosts select proteins containing aggregable peptide for the generation of pMHC clusters at the surface of presenting cells. Through mutations, some proteins of pathogens and cancer cells tend to converge towards the host 'near-self' that its T cells have auditioned to address.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46420983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MCP-1/CCR2 axis is involved in the regulation of γδT cells in lupus nephritis.","authors":"Ting Deng, Feifei Lei, Zhongyu Wang, Yangbin Wang, Gang Li, Yunhe Zhu, Boyu Du, Xueyan Xi","doi":"10.1111/sji.13305","DOIUrl":"10.1111/sji.13305","url":null,"abstract":"<p><p>γδT cells are important innate immune cells that are involved in the occurrence and development of autoimmune diseases such as systemic lupus erythematosus (SLE). Lupus nephritis (LN) is a serious complication of SLE, characterized by the accumulation of immune cells (including γδT cells) in the target organs to participate in the disease process. Therefore, clarifying how γδT cells chemotactically migrate to target organs may be a key to developing therapeutic methods against LN. Enzyme-linked immunosorbent assay (ELISA) was used to detect serum levels of chemokines in LN patients and healthy controls. Real-time polymerase chain reaction (RT-PCR) and flow cytometry were used to measure the expression of chemokine receptors on the surface of γδT cells. The chemotactic migration ability of γδT cells was detected by Transwell assay. Signalling pathway activation of γδT cells was detected by Automated Capillary Electrophoresis Immunoassay and flow cytometry. The serum levels of chemokines, including monocyte chemoattractant protein-1 (MCP-1) in LN patients, were significantly increased. CCR2, the receptor of MCP-1, was also highly expressed on the surface of peripheral γδT cells in LN patients. In addition, the exogenous addition of MCP-1 can enhance chemotactic migration of γδT cells in LN patients. MCP-1 could activate STAT3 signalling in LN patients' peripheral γδT cells. γδT cells might participate in the pathogenesis of LN through MCP-1/CCR2 axis. This finding provides new opportunities for developing treatment methods against LN by targeting MCP-1/CCR2 axis.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49127191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}