课程文献中心 更多>>

摘要： [Erratum to: BMB Reports 2025; 58(7): 307-312, PMID: 40495489, PMCID: PMC12313400] BMB Reports recently published the article "Modulating CD226 and PD-(L)1 pathways improves CMV-specific CD8＋T cell responses in the absence of IL-2" (BMB Rep. 2025; Vol. 58, No.7, pp.307-312) by Hye-In Sim et al. The original publication inadvertently omitted two sections: ACKNOWLEDGMENTS and CONFLICT OF INTEREST. These sections have now been added to the online version. The authors and editorial office apologize for any inconvenience or confusion this omission may have caused to the authors and readers. ACKNOWLEDGMENTS This work was supported by an intramural grant from KIST and Asan Medical Center (2022IP0092-1) and by grants from the National Research Foundation of Korea (NRF) (RS-2024-00338729 to H. Jin and RS-2024-00337093 to Y. Park). CONFLICT OF INTEREST All authors declare that they have no competing interests.

关键词： IL-10   aTCMR   NFATc1 signaling pathway   T cell   Kidney transplantation  

摘要： The cause of acute T cell-mediated rejection (aTCMR) is believed to be immune hyperfunction of T cells after kidney transplantation. Nowadays, calcineurin inhibitors are widely used to inhibit the proliferation of T cells when aTCMR occurs. However, the therapeutic dose window of these drugs is relatively narrow and long time use of these drugs may lead to serious side effects. Besides, whether IL-10, a new immune tolerance mediator, playing a therapeutic role on aTCMR remains unclear. The level of IL-10 decreased in patients with aTCMR, suggesting that IL-10 may be involved in the progression of aTCMR. IL-10 could inhibit the proliferation and metabolism of T cells in vitro and in vivo, accompanied by reducing the levels of IL-2, IFN-gamma, and TNF-alpha. Moreover, we confirmed that IL-10 exerts immunosuppressive effects by inhibiting the NFATc1 signaling pathway of T cells. This viewpoint may provide a new therapeutic idea for clinical application.

关键词： biopolymer   IL-12   immunotherapy   elastin-like polypeptide  

摘要： Despite renewed interest in IL-12 as a cancer immunotherapy due to its ability to stimulate the adaptive immune system, its short half-life and narrow therapeutic window continues to present challenges for effective delivery. Previous studies with IL-12 have investigated the effects of route of delivery or sustained delivery of the cytokine on its efficacy but are unable to simultaneously investigate the effects of both within the same system. This work seeks to address this gap by utilizing an elastin-like polypeptide (ELP) carrier, which can undergo a thermally triggered phase transition to a gel-like depot, to probe the effects of both sustained release and spatial delivery of IL-12. By conjugating IL-12 with an ELP, this work creates an IL-12-ELP fusion that can be injected intratumorally or subcutaneously to form a sustained-release depot. In a B16F10 murine model, intratumoral injection of a depot-forming IL-12-ELP fusion significantly improved survival compared to free IL-12. IL-12-ELP is retained within the tumor approximately fourfold longer than free IL-12, resulting in higher CD8+ T cell recruitment at the tumor and local concentrations of inflammatory cytokines at Day 2. Taken together, this work provides insights into rational cytokine delivery, the importance of tumor localization, and the benefits of sustained release.

摘要： *** most common cause of late graft failure in renal allotransplantation is chronic antibody-mediated rejection caused by donor-specific antibodies against class II human leukocyte antigen (HLA), particularly HLA-DQ. In preclinical renal xenotransplantation, graft failure 1-mo posttransplant is characterized by glomerulopathy and immunoglobulin G (IgG) staining in the glomerulus. Rhesus renal xenograft recipients with late graft failure also have anti-swine leukocyte antigen (SLA)-DQ antibodies present in their serum suggesting that, like allotransplantation, late xenograft failure may be driven by antidonor major histocompatibility complex class II antibodies, particularly SLA-DQ. Some patients have anti-SLA-DQ antibodies, but the magnitude of this problem is *** evaluated patient sera for the presence of anti-SLA-DQ antibodies in engineered immortalized cells, to determine patients' reactivity toward 7 different SLA-DQ molecules. Next, we created glycoprotein, alpha-galactosyltransferase 1/beta-1,4-N-acetyl-galactosaminyltransferase 2/SLA-DQ knockout (KO) pigs so that we could evaluate the impact of SLA-DQ on the level of antipig antibodies by performing crossmatches with serum from na & iuml;ve and HLA class II-sensitized patients and SLA-DQ KO peripheral blood mononuclear *** & iuml;ve and HLA class II-sensitized patients had anti-SLA-DQ immunoglobulin M and IgG that were pan-specific rather than SLA-DQ allele-specific. Crossmatching patient sera with peripheral blood mononuclear cells from the SLA-DQ KO pigs revealed that many patients had anti-SLA-DQ antibodies. Eliminating SLA-DQ reduced human immunoglobulin M and IgG binding to primary pig ***-DQ is a xenoantigen for most patients. SLA-DQ KO pigs may help address this problem.