Ask about this productRelated genes to: CD40L antibody
- Gene:
- CD40LG NIH gene
- Name:
- CD40 ligand
- Previous symbol:
- HIGM1, IMD3, TNFSF5
- Synonyms:
- CD40L, TRAP, gp39, hCD40L, CD154
- Chromosome:
- Xq26.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-04-23
Related products to: CD40L antibody
Related articles to: CD40L antibody
- Clinical xenotransplantation offers a conceptually unlimited supply of donor organs, owing to transformative advances in gene-editing technologies. However, the pharmacological and physiological distinctions between allo- and xenotransplantation pose a major challenge. Unlike allografts, xenografts simultaneously trigger complement-amplified humoral rejection, thromboregulatory incompatibility driven by porcine-human molecular mismatch, and species-specific innate inflammatory cascades. However, conventional calcineurin-based immunosuppression provides no meaningful coverage for these pathways. We analyzed these differences to provide the mechanistic foundation for a dedicated perioperative framework. The proposed framework encompasses immunologic assessment; porcine cytomegalovirus (PCMV)/roseolovirus-free donor certification; intensified induction; third-generation anti-CD154 monoclonal antibodies with pharmacokinetically verified trough targets; normothermic machine perfusion with anti-inflammatory perfusate supplementation; and thromboregulatory rescue protocols incorporating tranexamic acid, heparin, and antiplatelet agents. Furthermore, we aimed to address consumptive coagulopathy; targeted suppression of macrophage- and neutrophil-driven innate inflammatory cascades, alongside activation of xenoreactive natural killer cells; and multimodal surveillance integrating flow cytometry, donor-derived cell-free DNA, and metagenomic sequencing for porcine endogenous retrovirus and PCMV monitoring. By combining compassionate-use failure analysis with prospective trial design aligned with the 2026 International Society for Heart and Lung Transplantation consensus statement, this review proposes a standardized perioperative management protocol that is applicable to clinical xenotransplantation. - Source: PubMed
Publication date: 2026/09/22
Han Kyu-HyunYang Jaeseok - The essential role of B cells and B cell intrinsic molecules in tumor immunity is beginning to be recognized. Tumor cell CKLF-like MARVEL transmembrane domain-containing protein 6 (CMTM6) is a novel tumor immunoregulator involved in maintaining membrane levels of several important molecules, such as programmed cell death ligand 1 (PD-L1) and CD58. Host CMTM6 may also play a function in the tumor microenvironment. Here, we found that CMTM6 was highly expressed in splenic B cells and tumor-infiltrating B cells. CMTM6 deficiency resulted in impaired splenic development, germinal center B cell differentiation, memory B cell differentiation, T/B cell interaction and B cell anti-tumor immune responses. Through multi-omics data mining and B-cell agonist screening, we identified that CMTM6 interacted with CD40 and maintained CD40 membrane levels in B cells. CMTM6 -interacts with CD40 and inhibits ubiquitin/proteasome-mediated CD40 degradation. CMTM6 deficiency led to impaired CD40 signaling-mediated B cell activation, survival, proliferation, differentiation and T/B cell interaction. , CMTM6 deficiency leads to a significant decrease in the anti-tumor activity of immune checkpoint blockade (ICB) therapy and B cell-dependent CD40 agonists. Collectively, B-cell intrinsic CMTM6 maintains B cell CD40 levels and signaling to promote B cell function and anti-tumor immunity. - Source: PubMed
Publication date: 2026/07/15
Chen RunqiuChang WenlongLi FanglinGu LonghuaChen ChenZhang RongLi ZhiyingSun JianhuaChen JingGong LikunLong Yiru - Platelet activation plays a central role in arterial thrombosis, thromboinflammation, and microvascular injury. Conventional platelet function tests evaluate platelet responsiveness to exogenous agonists ex vivo but do not directly reflect in vivo platelet activation. Although several soluble platelet-derived molecules, including platelet factor 4 (PF4), β-thromboglobulin (β-TG), soluble P-selectin, soluble CD40 ligand, glycocalicin, and soluble glycoprotein (GP) VI, have been investigated as in vivo platelet activation markers, their clinical use is limited by preanalytical instability, lack of platelet specificity, constitutive shedding, or uncertain disease specificity. Soluble C-type lectin-like receptor 2 (sCLEC-2) has recently emerged as a promising biomarker of in vivo platelet activation. CLEC-2 is expressed predominantly in platelets and megakaryocytes, and its soluble form is released from activated platelets as both a shed molecule and a microparticle-associated form. Compared with PF4 and β-TG, sCLEC-2 is less susceptible to artifactual release during routine blood collection, making it more suitable for clinical laboratory testing. Elevated sCLEC-2 levels have been reported in acute coronary syndrome, acute ischemic stroke, disseminated intravascular coagulation, thrombotic microangiopathy, antiphospholipid antibody syndrome, and coronavirus disease 2019 (COVID-19). In thrombocytopenic disorders, indices incorporating platelet count, such as the C2PAC index, sCLEC-2/D-dimer ratio, and sCLEC-2 × D-dimer/platelet count, may better reflect platelet activation and disease status than sCLEC-2 concentration alone. However, preanalytical standardization, assay harmonization, reference interval validation, and disease-specific cutoff values remain essential. This review summarizes the biological basis, assay systems, clinical evidence, and future perspectives of sCLEC-2 as an emerging laboratory marker of in vivo platelet activation. - Source: PubMed
Publication date: 2026/08/28
Suzuki-Inoue KatsueUeda MakyoShirai ToshiakiTsukiji NagaharuSasaki Tomoyuki - Identifying genetic cause(s) is a key step for management and treatment of patients with inborn errors of immunity (IEI). Here, in an observational cross-sectional genomic study, we analyzed whole-genome sequencing (WGS) data of 72 IEI patients from Saint Petersburg and Northwestern Russia: 42 patients with common variable immunodeficiency (CVID)-like phenotypes, 6 patients with clinically diagnosed X-linked agammaglobulinemia (XLA or Bruton's disease), and 24 patients with other forms of IEI. Causative pathogenic and likely pathogenic variants in , , , , , , , and genes were identified in 14 (19%) patients. Variants of uncertain significance that could be linked to observed clinical phenotypes were detected in 6 patients. These included a variant in a patient with Bruton's disease, variants in , , and in patients with CVID, and variants in and in patients with other forms of IEI. Additional rare variants that were mostly unique to individual patients were found in multiple IEI genes from the International Union of Immunological Societies (IUIS) Expert Committee 2024 list. In the CVID-like subcohort, pathway-level analysis of these rare variants revealed patterns associated with clinical manifestations. Taken together, our results expand the genetic characterization of an understudied regional IEI cohort, particularly of patients with CVID-like phenotypes, and identify genetic factors that are implicated in or may contribute to the disease. - Source: PubMed
Publication date: 2026/09/05
Petrusenko YunnaSavin TikhonSedykh AnnaChekanov NikolayKlimuk EvgenyOstankova YuliaKuznetsova RaisaChernyshova AnnaMilichkina AnzhelikaTotolian AregSeverinov Konstantin - X-linked hyper-immunoglobulin M (XHIGM) syndrome is a rare primary immunodeficiency caused by mutations in the CD40 ligand gene , characterized by defective T-cell-dependent B-cell class-switch recombination. Patients typically present with recurrent infections in early childhood, but diagnosis is often delayed due to heterogeneous clinical manifestations and the fact that serum IgM levels may remain within the normal range in a significant proportion of patients. Here we report a case of XHIGM in an infant whose diagnostic journey began with recurrent lymphadenitis and culminated in life-threatening pneumonia (PJP). - Source: PubMed
Publication date: 2026/08/26
Guo YingHe XiaoliZhang LijunLi MengtingHe LuluLu Guoyan