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This Research Topic honors the memory of Prof. Antonius “Ton” G. Rolink (April 19, 1953–August 06, 2017), our colleague, mentor and friend in immunology. It is now over a year since Ton left us. This article collection, authored by many of Ton’s friends and colleagues, reflects the huge contribution to cellular and molecular immunology that work emanating directly from Ton’s own hands and laboratory have made to the understanding of lymphocyte development. Ton’s hard work, expertise, generosity, passion for science and infectious humor were legendary and for all of those lucky enough to have been his colleague, he ensured that science was fun. We take this opportunity of thanking all contributors for submitting their manuscripts; we are sure that Ton would have enjoyed reading and making his own insightful comments on them. In the form of original research and review articles, these papers cover many of Ton’s scientific interests in different aspects of lymphocyte development in mouse and man. In the first section, Development of hematopoietic cells and lymphocytes, Klein et al. describe the accumulation of multipotent hematopoietic progenitors in peripheral lymphoid organs of IL-7xFlt3L double transgenic mice and Pang et al. the role of the transcription factor PU.1 on the development of Common Lymphoid Progenitors. In Early B cell development, Winkler and Mårtensson review the role of the Pre-B cell receptor in B cell development and papers by Hobeika et al. and Brennecke et al. describe models of inducible B cell development. For B cell selection, survival and tolerance, Smulski and Eibel review the role of BAFF and Kowalczyk-Quintans et al. analyse the role of membrane-bound BAFF. The impact of BIM on B cell homeostasis is discussed by Liu et al. The role of the MEK-ERK pathway in B cell tolerance is discussed by Greaves et al. and the transcriptional regulation of germinal center development is reviewed by Song and Matthias. For Hematological diseases, Ghia reviews how studies of B cell development help the understanding of Leukemia development, Kim and Schaniel review how iPS technology helps the understanding of hematological diseases and Hellmann et al. describe development of new therapeutic antibody drug conjugates. Finally, in T cell development, homeostasis and graft vs. host disease, Heiler et al. describe the therapeutic effects of IL-2/anti-IL-2 immune complexes in GvHD, Calvo-Asensio et al. describe the DNA damage response of thymocyte progenitors and Mori and Pieters review the role of Coronin 1 in T cell survival.

T cell development --- B cell selection and survival --- BAFF --- Cytokines --- IPSC --- Leukemia --- T cell survival --- Transcription Factors --- B cell development --- Hematopoietic Stem Cells

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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

3D cell culture --- biomaterial disease models --- Neuron --- neurodegeneration --- tumor --- Blood Brain Barrier (BBB) --- Brain Disorders --- Hydrogels --- iPSC = induced pluripotent stem cell --- Bioprinting

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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

Civil engineering, surveying & building --- Mechanical engineering & materials --- 3D cell culture --- biomaterial disease models --- Neuron --- neurodegeneration --- tumor --- Blood Brain Barrier (BBB) --- Brain Disorders --- Hydrogels --- iPSC = induced pluripotent stem cell --- Bioprinting --- 3D cell culture --- biomaterial disease models --- Neuron --- neurodegeneration --- tumor --- Blood Brain Barrier (BBB) --- Brain Disorders --- Hydrogels --- iPSC = induced pluripotent stem cell --- Bioprinting

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It has been more than 25 years since the identification of the FMR1 gene and the demonstration of the causative role of CGG-repeat expansion in the disease pathology of fragile X syndrome (FXS), but the underlying mechanisms involved in the expansion mutation and the resulting gene silencing still remain elusive. Our understanding of the pathways impacted by the loss of FMRP function has grown tremendously, and has opened new avenues for targeted treatments for FXS. However, the failure of recent clinical trials that were based on successful preclinical studies using the Fmr1 knockout mouse model has forced the scientific community to revisit clinical trial design and identify objective outcome measures. There has also been a renewed interest in restoring FMR1 gene expression as a possible treatment approach for FXS. This special issue of Brain Sciences highlights the progress that has been made towards understanding the disease mechanisms and how this has informed the development of treatment strategies that are being explored for FXS.

n/a --- lymphoblast --- pluripotent stem cells --- FMR1 --- Gene editing --- X chromosome --- Fmr1 --- epigenetic gene silencing --- FMR1 gene --- Fragile X syndrome 1 --- repeat instability --- characteristics that have the greatest impact --- DNA instability --- working memory --- language development --- mosaicism --- CRISPR 3 --- clinical trials --- autism spectrum disorders --- Fmr1 KO mouse --- automated vocal analysis --- base excision repair (BER) --- inhibitory control --- cerebral spinal fluid --- iPSC --- drug development --- targeted treatments --- molecular biomarkers --- viral vector --- avoidance --- biomarker --- set-shifting --- early identification --- expansion --- anxiety --- planning --- voice of the person --- mismatch repair (MMR) --- gene reactivation --- double-strand break repair (DSBR) --- newborn screening --- intellectual disability --- processing speed --- voice of the patient --- fragile X syndrome --- adeno-associated virus --- neurodevelopmental disorders --- histone methylation --- Non-homologous end-joining (NHEJ) --- ASD --- Fxr2 --- Fragile X-associated Tremor/Ataxia Syndrome 2 --- Trinucleotide Repeat 4 --- CGG Repeat Expansion Disease --- DNA methylation --- contraction --- fragile X mental retardation protein --- RNA:DNA hybrid --- behavior --- developmental disorders --- cognition --- females --- FMRP --- Fragile X Syndrome --- unstable repeat diseases --- protein synthesis --- brain --- cognitive flexibility --- treatment development --- fibroblast --- PRC2 --- transcription coupled repair (TCR) --- best practices --- attention --- Fragile X --- executive function