Results and Problems in Cell Differentiation最新文献_第2页

How Cytokines Regulate Immune Response Toward Chronic Allograft Rejection? 细胞因子如何调节慢性同种异体移植排斥反应的免疫反应？

Results and Problems in Cell Differentiation Pub Date : 2026-01-01 DOI: 10.1007/978-3-032-07686-1_2

Stanislaw Stepkowski, Jared Oenick, Dulat Bekbolsynov, Beata Mierzejewska, Michael Rees, Obi Ekwenna

{"title":"How Cytokines Regulate Immune Response Toward Chronic Allograft Rejection?","authors":"Stanislaw Stepkowski, Jared Oenick, Dulat Bekbolsynov, Beata Mierzejewska, Michael Rees, Obi Ekwenna","doi":"10.1007/978-3-032-07686-1_2","DOIUrl":"10.1007/978-3-032-07686-1_2","url":null,"abstract":"Intensive research for 50 years did not find a way to predict the faith of organ transplants after successful transplantation. Current immunosuppressive regiments reduce kidney transplant acute rejection episodes to 6-11% for the first year, but 49% of them develop chronic allograft nephropathy in 5 years. Similarly, heart transplants have 8% acute rejection episodes in the first year and 50% develop cardiac vasculopathy in 5 years. Multiple cytokines regulate acute cellular T-cell-mediated rejection (TCMR) and acute antibody-mediated rejection (AMR), and both mechanisms contribute to chronic allograft rejection. In addition to common γ chain (cγ) cytokines [interleukin-2 (IL-2), IL-4, IL-7, IL-9, IL-15, and IL-21], other cytokines [IL-1, IL-6, IL-10, interferon-α, (IFN)α, INFβ, INFγ, tumor necrosis factor α, TNFα; tumor growth factor β, TGFβ] are all extensively involved in the regulation of acute and chronic allograft rejections. Interestingly, the same cytokines also regulate functions of normal cells and tissues. To induce transplant tolerance, it is necessary to maintain physiological cytokine levels as well as boost the function of T regulatory T (Treg) cells producing IL-10, IL-35, and TGFβ. This chapter emphasizes the necessity of maintaining a balance by cytokines to divert them from the inflammation path producing chronic rejection to normal function support combined with Treg-dominated transplantation tolerance.","PeriodicalId":39320,"journal":{"name":"Results and Problems in Cell Differentiation","volume":"77 ","pages":"25-70"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145890345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cellular and Molecular Aspects of Chronic Rejection. 慢性排斥反应的细胞和分子方面。

Results and Problems in Cell Differentiation Pub Date : 2026-01-01 DOI: 10.1007/978-3-032-07686-1_1

Zhongcheng Mei, Alexander Sasha Krupnick

引用次数: 0

Chronic Rejection in Facial Vascularized Composite Allotransplantation (fVCA). 面部血管化复合异体移植（fVCA）的慢性排斥反应。

Results and Problems in Cell Differentiation Pub Date : 2026-01-01 DOI: 10.1007/978-3-032-07686-1_10

Felix J Klimitz, Leonard Knoedler, Samuel Knoedler, Bohdan Pomahac, Martin Kauke-Navarro

{"title":"Chronic Rejection in Facial Vascularized Composite Allotransplantation (fVCA).","authors":"Felix J Klimitz, Leonard Knoedler, Samuel Knoedler, Bohdan Pomahac, Martin Kauke-Navarro","doi":"10.1007/978-3-032-07686-1_10","DOIUrl":"https://doi.org/10.1007/978-3-032-07686-1_10","url":null,"abstract":"Chronic rejection (CR) remains a major barrier to long-term success in facial vascularized composite allotransplantation (fVCA), particularly in facial transplants. Unlike acute rejection, CR is a gradual, progressive process marked by vasculopathy, fibrosis, and functional graft decline. Histopathologic features include intimal hyperplasia, dermal sclerosis, adnexal atrophy, and telangiectasia. Immune mechanisms driving CR involve persistent activation of Th1 and Th17 T cells, macrophages, and, to a lesser extent, B cells, which form tertiary lymphoid structures. Dysregulated cytokines and chemokines, such as IFN-γ, IL-17, and IL-6, perpetuate inflammation and fibrosis, whereas the downregulation of regulatory mediators like IL-10 impairs immune resolution. Chronic antigen exposure, complement activation, and the presence of tissue-resident memory T cells further sustain graft injury. Clinically, CR presents with tightening of facial tissue, pigmentary changes, pain, and impaired oral and facial function, which can sometimes progress to necrosis and graft failure. Diagnostic challenges persist due to heterogeneous presentation and a lack of standardized criteria. Early detection through protocol biopsies, mucosal sampling, and vascular imaging is essential. Future directions emphasize the need for molecular diagnostics, targeted immunomodulation, and antifibrotic therapies. A deeper understanding of CR pathophysiology is critical to improving graft longevity and patient quality of life in fVCA.","PeriodicalId":39320,"journal":{"name":"Results and Problems in Cell Differentiation","volume":"77 ","pages":"201-221"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145890397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Epigenetic Echoes: Decoding the Acetylation Journey from Neural Crest to Melanocyte. 表观遗传回声：解码从神经嵴到黑素细胞的乙酰化过程。

Results and Problems in Cell Differentiation Pub Date : 2025-01-01 DOI: 10.1007/978-3-031-91459-1_7

Ayesha Nasreen, Sribas Chowdhury, Dharani Alagar Selvam, Vivek T Natarajan

{"title":"Epigenetic Echoes: Decoding the Acetylation Journey from Neural Crest to Melanocyte.","authors":"Ayesha Nasreen, Sribas Chowdhury, Dharani Alagar Selvam, Vivek T Natarajan","doi":"10.1007/978-3-031-91459-1_7","DOIUrl":"https://doi.org/10.1007/978-3-031-91459-1_7","url":null,"abstract":"Epigenetic mechanisms influence early developmental events, shaping gene expression in exciting ways that go beyond the DNA blueprint. The state of chromatin is governed by an interplay between various histone modifications, variants, nucleosome remodeling complexes, and other chromatin modifiers that work in sync to prime the chromatin for specific biological outcomes. In this chapter, we explore neural crest cells (NCCs), a critical progenitor population that retains the extensive developmental potential of their blastula origins. The formation and differentiation of NCCs into diverse cell types are influenced by the regulation of their acetylation state through various epigenetic factors. This chapter delves into the intricate interplay between histone acetylases (HATs) and deacetylases (HDACs), highlighting how these enzymes modify chromatin to create a permissive environment for the induction of NCCs and steer their fate toward the melanocytic lineage. The shift in acetylation profiles during the transition from melanocytes to melanoma suggests that the transcriptional machinery may override normal regulatory mechanisms, promoting a neural crest-like state in melanoma development. Epigenetic regulation, particularly through histone acetylation, plays a pivotal role in neural crest cell development and melanoma initiation offering potential therapeutic targets.","PeriodicalId":39320,"journal":{"name":"Results and Problems in Cell Differentiation","volume":"75 ","pages":"189-209"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144545322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Impact of Histone Acetyltransferases and Histone Deacetylases on Adult Brain Myelin Plasticity. 组蛋白乙酰转移酶和组蛋白去乙酰化酶对成人脑髓磷脂可塑性的影响。

Results and Problems in Cell Differentiation Pub Date : 2025-01-01 DOI: 10.1007/978-3-031-91459-1_8

Alessandra Dominicis, Tommaso Fabiano, Simone Peria, Aland Ibrahim Ahmed Al Jaf, Antonella Ragnini-Wilson

{"title":"Impact of Histone Acetyltransferases and Histone Deacetylases on Adult Brain Myelin Plasticity.","authors":"Alessandra Dominicis, Tommaso Fabiano, Simone Peria, Aland Ibrahim Ahmed Al Jaf, Antonella Ragnini-Wilson","doi":"10.1007/978-3-031-91459-1_8","DOIUrl":"https://doi.org/10.1007/978-3-031-91459-1_8","url":null,"abstract":"Myelin plasticity is a key process for acquiring new motor skills and preventing neurodegeneration during ageing. Neural precursor cells (NPCs) and parenchymal oligodendrocyte precursor cells (OPCs) play a key role in myelin plasticity in the central nervous system (CNS), being specialized in reconstituting the myelin sheath upon damage. Reversible acetylation, regulated by histone acetyltransferases (HATs) and histone deacetylases (HDACs) activity, controls these stem cells' differentiation in myelinating oligodendrocytes (mOLs) during their proliferation and remyelination processes. By modulating cytosolic protein activity and precisely orchestrating the spatial and timely regulated activity of the transcription factors participating in the NPC and OPC differentiation process, these enzymes play a vital role in preserving the adult brain's cognitive capacity during ageing. This review highlights the role of reversible acetylation in the regulation of stem cell differentiation during remyelination, as disruptions in this process contribute to severe neurodegenerative impairments and accelerated ageing.","PeriodicalId":39320,"journal":{"name":"Results and Problems in Cell Differentiation","volume":"75 ","pages":"213-246"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144545324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Acetylation-Mediated Epigenetic Consequences for Biological Control and Cancer. 乙酰化介导的表观遗传后果的生物控制和癌症。

Results and Problems in Cell Differentiation Pub Date : 2025-01-01 DOI: 10.1007/978-3-031-91459-1_2

Andrew J Fritz, Kyle T McKay, Haley W Greenyer, Emory Pacht, Rabail H Toor, Rahim Ullah, Jackson R Del Porto, Abigail G Person, Sadie J Korzec, Kathleen E Bright, Genevieve Brzoza, Jessica L Heath, Prachi N Ghule, Jonathan A R Gordon, Andre J Van Wijnen, Seth E Frietze, Karen C Glass, Jane B Lian, Janet L Stein, Gary S Stein

引用次数: 0

Histone and Non-histone Reversible Acetylation in Development, Aging, and Disease. 组蛋白和非组蛋白可逆乙酰化在发育、衰老和疾病中的作用。

Results and Problems in Cell Differentiation Pub Date : 2025-01-01 DOI: 10.1007/978-3-031-91459-1_1

Sezgin Gunes, Neslihan Hekim, Sercan Ergun, Elzem Nisa Alkan, Cansu Can

引用次数: 0

Tubulin Acetylation and the Cellular Mechanosensing and Stress Response. 微管蛋白乙酰化与细胞机械感应和应激反应。

Results and Problems in Cell Differentiation Pub Date : 2025-01-01 DOI: 10.1007/978-3-031-91459-1_5

Bruno Carmona, Inês L S Delgado, Sofia Nolasco, Rita Marques, João Gonçalves, Helena Soares

{"title":"Tubulin Acetylation and the Cellular Mechanosensing and Stress Response.","authors":"Bruno Carmona, Inês L S Delgado, Sofia Nolasco, Rita Marques, João Gonçalves, Helena Soares","doi":"10.1007/978-3-031-91459-1_5","DOIUrl":"https://doi.org/10.1007/978-3-031-91459-1_5","url":null,"abstract":"Microtubule (MT) acetylation has emerged as a critical regulator of cellular stress responses, integrating mechanical and oxidative stimuli to support cellular adaptability and survival. This post-translational modification (PTM) enhances MT flexibility and resilience, enabling cells to withstand mechanical challenges such as changes in extracellular matrix stiffness and applied forces. Through its impact on MT physical properties, acetylation minimizes cytoskeletal breakage, reducing the need for constant remodeling and supporting cellular integrity under mechanical stress. Furthermore, tubulin acetylation regulates intracellular trafficking by modulating interactions with molecular motors, allowing for efficient cargo transport and precise spatial organization without disrupting the MT network. In the context of oxidative stress, tubulin acetylation responds to redox imbalances by stabilizing MTs and influencing cellular pathways that regulate reactive oxygen species (ROS). This modification is linked to enhanced antioxidant responses, autophagy regulation, and mitochondrial dynamics, highlighting its role in maintaining cellular homeostasis under oxidative conditions. The dual function of tubulin acetylation, responding to and integrating signals from mechanical and oxidative stress, acts as a bridging mechanism between physical and chemical signaling pathways. Consequently, it has the potential to be a therapeutic target in diseases characterized by dysregulated stress responses, including neurodegenerative disorders, cancer, and cardiovascular conditions. Despite significant progress has been made, unanswered questions persist, particularly regarding the molecular mechanisms by which acetylated MTs encode spatial and functional information and their interplay with other tubulin PTMs.","PeriodicalId":39320,"journal":{"name":"Results and Problems in Cell Differentiation","volume":"75 ","pages":"141-162"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144545330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Acetylation and Deacetylation of Cytoskeleton-Associated Proteins. 细胞骨架相关蛋白的乙酰化和去乙酰化。

Results and Problems in Cell Differentiation Pub Date : 2025-01-01 DOI: 10.1007/978-3-031-91459-1_3

Dale D Tang

引用次数: 0

Acetylation in Viral Infection and Disease. 乙酰化在病毒感染和疾病中的作用。

Results and Problems in Cell Differentiation Pub Date : 2025-01-01 DOI: 10.1007/978-3-031-91459-1_12

Matloob Husain

{"title":"Acetylation in Viral Infection and Disease.","authors":"Matloob Husain","doi":"10.1007/978-3-031-91459-1_12","DOIUrl":"https://doi.org/10.1007/978-3-031-91459-1_12","url":null,"abstract":"Viruses are acellular organisms and part of our ecosystem but exist at the interface of living and non-living. Furthermore, viruses are obligate intracellular parasites hence require the machinery of other organisms to multiply. Consequently, most viral infections result into a viral disease. Broadly, viruses cause two types of infection-acute and persistent (latent and chronic), in humans and other mammals that could lead to various lethal and non-lethal viral diseases. Acetylation is now known to be a ubiquitous protein (and nucleic acid) modification and is critical for cellular metabolism. An imbalance in acetylation has been associated with various cancers and diseases in humans. Likewise, the association of acetylation with viral infection and disease was observed soon after its discovery in twentieth century. Now, the literature accumulated in this space shows that acetylation promotes the infection of many viruses causing both acute and persistent infections. Furthermore, reduction in the acetylation level reduces viral clearance from the host and promotes viral persistency. The latter can be interrupted by increasing the acetylation level by using deacetylase inhibitors. Indeed, this approach has become a therapeutic tool to treat and clear the persistent viral infections as well as boost the oncolytic virus-mediated cancer therapy.","PeriodicalId":39320,"journal":{"name":"Results and Problems in Cell Differentiation","volume":"75 ","pages":"329-361"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144545319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0