Ask about this productRelated genes to: CD38 antibody
- Gene:
- CD38 NIH gene
- Name:
- CD38 molecule
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4p15.32
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2014-11-18
Related products to: CD38 antibody
Related articles to: CD38 antibody
- Although bone marrow-derived mesenchymal stem cell (BMSC) offers considerable therapeutic potential, the regenerative capacity of these cells is markedly compromised by the adverse microenvironment of the injured liver. Hypoxic preconditioning (HP) enhances the adaptability of BMSC. This study explored HP-BMSC therapy for acute liver failure (ALF), specifically examining the potential regulatory effects involving the VEGF-related factors and B-cell immunity. - Source: PubMed
Publication date: 2026/05/21
Lan Mei-MeiShi Rui-ZhiLi Zhe-YuQiao Wen-JunGuan Yong-JuanHe Wen-QiangLi Jun-FengZhang Li-Ting - Immunomodulatory drugs (IMiDs), including lenalidomide and pomalidomide in combination with proteasome inhibitors, dexamethasone and anti-CD38 monoclonal antibodies, play a central role in the treatment of multiple myeloma (MM) across newly diagnosed and relapsed stages. These treatment regimens have significantly improved patient outcomes worldwide, establishing IMiDs as one of the backbones of MM therapy. A new generation of more potent compounds called cereblon E3 ligase modulators (CELMoDs) is now being developed to potentially replace the older IMiDs. In addition, novel immunotherapeutic approaches led by chimeric antigen receptor (CAR T), T-cell engagers and antibody-drug conjugates are also increasingly used in relapsed and refractory myeloma patient care. However, despite these advances, resistance to IMiD-based therapies inevitably develops and represents a major clinical challenge. Understanding the biological basis of resistance to IMiD-based therapy is crucial to plan and maximise treatment options for patients when they relapse on IMiD containing regimens. Emerging evidence underscores the role of genetic and epigenetic alterations, changes in downstream signalling, and dysregulation of the bone marrow immune microenvironment in driving therapeutic resistance. In this review, we explore current literature on the molecular and immune mechanisms related to the onset of therapeutic resistance. We then suggest ways to overcome resistance and exemplify options for the future, focusing on immunotherapy combinations with IMiDs or CELMoDs and novel agents. - Source: PubMed
Publication date: 2026/05/21
Fuentes-Lacouture Maria-CynthiaNandana DeviRamasamy KarthikThakurta Anjan - Micronutrients serve as critical metabolic sensors and epigenetic regulators that orchestrate cytokine production through multiple overlapping signalling cascades, transcriptional networks, and cellular metabolic states. This comprehensive review synthesizes recent research demonstrating that micronutrient status regulates cytokine biology at five hierarchical levels: (i) nutrient sensing via mTORC1/GCN2 and amino acid sensor networks; (ii) transcriptional control through VDR/RARĪ±-mediated epigenetic remodelling and histone deacetylase inhibition; (iii) redox signalling via SELENOK/selenoprotein-stabilized calcium homeostasis and Nrf2/ARE pathway activation; (iv) Pyroptosis/ferroptosis execution via metallothionein-zinc-caspase axes and NLRP3/GSDMD regulation; and (v) metabolic bioenergetics through NAD+/CD38/SIRT-mediated immune cell differentiation and aging. Recent discoveries establish that vitamin D directly suppresses IL-22 through repressive VDREs independent aryl-hydrocarbon receptor (AhR) signalling, zinc-metallothionein-3 that suppresses non-canonical inflammasome activation via TRIF-IRF3-STAT1 modulation, selenium-dependent SELENOK which stabilizes IP3 receptor-mediated store-operated calcium entry in immune cells, and folate-dependent one-carbon metabolism generating S-adenosyl methionine (SAM) that tunes epigenetic landscapes of cytokine genes. This review compiles the integrated mechanistic frameworks linking micronutrient availability to immunometabolic checkpoints, with implications for nutritional immunotherapy in chronic inflammatory diseases and immune-senescence. - Source: PubMed
Publication date: 2026/05/05
Ghosh JoyetaChattopadhyay Debprasad - - Source: PubMed
Publication date: 2026/05/21
Neumann FrankSchormann ClaudiaCetin OnurKos Igor ABewarder MoritzSchwarz Eva CLohse StefanMaurer StephanieStaber Philipp BBittenbring Joerg TSmola SigrunChristofyllakis KonstantinosHoth MarkusThurner Lorenz - Monocyte exhaustion is a dysfunctional immune state marked by persistent inflammation and immune suppression, reflected in STAT1-mediated expression of pathogenic inflammatory mediator CD38 and immune suppressive PD-L1, as well as a suppression of Akt signaling and a reduction of immune-enhancing mediator CD86. While prolonged Toll-like receptor 4 (TLR4) stimulation induces monocyte exhaustion, the roles of other TLRs remain unclear. Here, we systematically evaluated the ability of TLR-2, TLR-3, TLR-7, and TLR-9 agonists to induce murine bone marrow-derived monocytes exhaustion in vitro. Although all tested agonists promoted exhaustion phenotypes to varying degrees, characterized by upregulation of STAT1 mediated expression of CD38 and PD-L1, only TLR-2 and TLR7 agonists drastically suppressed Akt and CD86. In contrast, TLR-3 or TLR-9 agonists preferentially sustained Akt activation and CD86 expression. Mechanistically, STAT1/STAT3 activation mediated by mTROC1 was common across TLR agonists responsible for elevated expression of CD38 and PD-L1. On the other hand, Akt signaling mediated by mTORC2 responsible for the expression of CD86 was preferentially suppressed by TLR-2 and TLR-7 agonists, but retained by TLR-3 and TLR-9 agonists. Deletion of Rictor, a key component of mTORC2, blocked the activation of Akt/CD86 triggered by TLR-3/9 agonists, and further elevated mTORC1 mediated activation of STAT1/3 as well as CD38 expression. Conversely, Fumagillin or Rapamycin treatment, which has been associated with reduced mTORC1 signaling activity, mitigated TLR-2/7-induced STAT1/STAT3 activation and CD38 expression. These findings reveal that monocyte exhaustion is a shared but differentially regulated outcome of distinct TLR pathways, with the mTOR axis potentially serving as a key therapeutic target for immune dysfunction. - Source: PubMed
Publication date: 2026/05/20
Wang JingWu YajunLee GraceRazani BabakLi Liwu