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Based on gene annotation and non-synonymous single-nucleotide polymorphisms (SNPs) in the major SWand SL-associated regions, we found that two genes encoding a VQ motif and an E3 ubiquitin-protein ligase may be candidate genes influencing SL, while an F-box and leucinerich repeat (LRR) domain-containing protein is the potential regulator for SW in C. maxima. This study provides the first high-density linkage map of C. maxima using SNPs developed by SLAF-seq technology, which is a powerful tool for associated mapping of important agronomic traits, map-based gene cloning and marker-assisted selection (MAS)-based breeding in C. PTX inhibitor maxima. Copyright © 2020 Wang, Wang, Han, Luo, Wang, Yan, Xu and Qu.Phytoliths in the inflorescence of Poaceae plants can be of high taxonomic value in some archaeological contexts and provide insight into plant taxonomy and crop domestication processes. In this study, phytoliths in every inflorescence bract of 38 common Panicoideae weeds and minor crops in China were studied. Based on dissection of the inflorescence into different bracts using a treatment that retained the phytoliths anatomical position, observations of inflorescence phytoliths types and distribution were described in detail. We found that Interdigitating, Blocky amoeboid, Rectangular dentate, and Elongate dendritic with multi tent-like arch tops were of higher taxonomic value than the other types in our studied species. Both morphological and morphometric traits of the Interdigitating were summarized and compared with previous studies; the findings suggested that genus level discrimination of some Paniceae species could be reliable, and tribe/species level discrimination might be feasible. The phytoliths in the involucre of domesticated and wild type Coix lacryma-jobi provided insight into the domestication process of this plant. Our data also indicated that phytolith production in the inflorescence bracts might be under the genetic and molecular control of inflorescence development. Thus, the findings of this study could assist future studies in plant taxonomy and archaeobotany. Copyright © 2020 Ge, Lu, Zhang, Wang and Gao.MICA and MICB are ligands of the NKG2D receptor and thereby influence NK and T cell activity. MICA/B gene polymorphisms, expression levels and the amount of soluble MICA/B in the serum have been linked to autoimmune diseases, infections, and cancer. In hematopoietic stem cell transplantation, MICA matching between donor and patient has been correlated with reduced acute and chronic graft-vs.-host disease and improved survival. Hence, we developed an extremely cost-efficient high-throughput workflow for genotyping MICA/B for newly registered potential stem cell donors. Since mid-2017, we have genotyped over two million samples using NGS amplicon sequencing for MICA/B exons 2-5. In donors of German origin, MICA*008 is the most common MICA allele with a frequency of 42.3%. It is followed by MICA*002 (11.7%) and MICA*009 (8.8%). The three most common MICB alleles are MICB*005 (43.9%), MICB*004 (21.7%), and MICB*002 (18.9%). In general, MICB is less diverse than MICA and only 6 alleles, instead of 15, account for a cumulative allele frequency of 99.5%. In 0.5% of the samples we observed at least one allele of MICA or MICB which has so far not been reported to the IPD/IMGT-HLA database. By providing MICA/B typed voluntary donors, clinicians become empowered to include MICA/B into their donor selection process to further improve unrelated hematopoietic stem cell transplantation. Copyright © 2020 Klussmeier, Massalski, Putke, Schäfer, Sauter, Schefzyk, Pruschke, Hofmann, Fürst, Carapito, Bahram, Schmidt and Lange.Acute ischemic stroke (AIS) is common in patients with cancer, and mounting clinical evidence suggests that it may shorten the survival of cancer patients. But how stroke affects the progression of cancer remains unclear. link2 We inoculated B16 tumor cells (2 × 105) subcutaneously before distal middle cerebral artery occlusion (dMCAO) or sham surgery in C57BL/6 mice and found that compared to sham operated mice, dMCAO mice developed significantly increased tumor volume and were accompanied by lower survival rate. To explore the underlying mechanism, we performed RNA-sequencing analysis of the tumor tissue from mice with or without stroke and found prominent upregulation of lipocalin 2 (LCN2) in the tumor from stroke mice compared to those from sham mice. Using quantitative reverse transcription-PCR, we confirmed increased mRNA expression of LCN2 as well as anti-inflammatory cytokines-Arg1, IL-10, and decreased mRNA level of pro-inflammatory cytokines-IL-6, IL-23 in the tumor of cancer-bearing stroke mice. Both immunofluorescence staining and flow cytometry analysis revealed that increased expression of LCN2 was mainly derived from the polymorphonuclear myeloid derived suppressor cells (PMN-MDSCs) in the tumor. We also found that stroke reduced the PMN-MDSCs in the peripheral blood, but increased PMN-MDSCs in the tumor of the cancer-bearing mice after stroke. In conclusion, cerebral ischemic stroke may exacerbate cancer progression by increasing LCN2 expression in PMN-MDSCs, which turns out to be a promising therapeutic target to suppress cancer progression after ischemic stroke. link3 Copyright © 2020 Huang, Li, Zhou, Lu, Zhang, Tang, Gan, He, Chen, Yu and Li.Natural killer (NK) cells are the most abundant lymphocytes at the maternal-fetal interface. Epidemiological data implicate NK cells in human pregnancy outcomes. Discoveries using mouse NK cells have guided subsequent advances in human NK cell biology. However, it remains challenging to identify mouse and human uterine NK (uNK) cell function(s) because of the dynamic changes in the systemic-endocrinological and local uterine structural microenvironments during pregnancy. This review discusses functional similarities and differences between mouse and human NK cells at the maternal-fetal interface. Copyright © 2020 Sojka.Although there is evidence that autoimmune diseases share similar immunogenetic mechanisms, studies comparing peripheral CD45+ cells from patients with autoimmune endocrine diseases in parallel are limited. In this study, we applied high-dimensional single-cell mass cytometry to phenotypically characterize PBMC from patients with new-onset (N-T1D) and long-standing type 1 diabetes, Hashimoto's thyroiditis (HT), Graves' disease and autoimmune Addison's disease (AD), as well as healthy controls. The frequency of CD20loCD27hiCD38hiHLA-DRint plasmablasts, CD86+CD14loCD16+ non-classical monocytes and two subsets of CD56dimHLA-DR+IFN-γ+ NK cells were increased in patients with HT. Subsets of CD56dimCD69+HLA-DR- NK cells and CD8+ TEMRA cells, both expressing IFN-γ, were expanded and reduced, respectively, in the N-T1D group. In addition, patients with AD were characterized by an increased percentage of central memory CD8+ T cells that expressed CCR4, GATA3, and IL-2. We demonstrate that patients with N-T1D, HT, and AD had altered frequencies of distinct subsets within antigen-presenting and cytotoxic cell lineages. Previously unreported alterations of specific cell subsets were identified in samples from patients with HT and AD. Our study might contribute to a better understanding of shared and diverging immunological features between autoimmune endocrine diseases. Copyright © 2020 Magnusson, Barcenilla, Pihl, Bensing, Espes, Carlsson and Casas.Chikungunya virus (CHIKV) is an arthropod-borne alphavirus that causes hallmark debilitating polyarthralgia, fever, and rash in patients. T cell-mediated immunity, especially CD4+ T cells, are known to participate in the pathogenic role of CHIKV immunopathology. The other T cell subsets, notably CD8+, NKT, and gamma-delta (γδ) T cells, can also contribute to protective immunity, but their effect is not actuated during the natural course of infection. This review serves to consolidate and discuss the multifaceted roles of these T cell subsets during acute and chronic phases of CHIKV infection, and highlight gaps in the current literature. Importantly, the unique characteristics of skin-resident memory T cells are outlined to propose novel prophylactic strategies that utilize their properties to provide adequate, lasting protection. Copyright © 2020 Poh, Chan and Ng.[This corrects the article DOI 10.3389/fimmu.2019.02870.]. Copyright © 2020 Li, Wang, Cao, Bao, Li, Sun, Bai, Fu, Ma, Zhang, Li, Chen, Liu, An, Wu, Lu and Liu.Atherosclerosis, a chronic inflammatory disease of the arterial wall, is among the leading causes of morbidity and mortality worldwide. The persistence of low-grade vascular inflammation has been considered to fuel the development of atherosclerosis. However, fundamental mechanistic understanding of the establishment of non-resolving low-grade inflammation is lacking, and a large number of atherosclerosis-related cardiovascular complications cannot be prevented by current therapeutic regimens. Trained immunity is an emerging new concept describing a prolonged hyperactivation of the innate immune system after exposure to certain stimuli, leading to an augmented immune response to a secondary stimulus. While it exerts beneficial effects for host defense against invading pathogens, uncontrolled persistent innate immune activation causes chronic inflammatory diseases. In light of the above, the long-term over-activation of the innate immune system conferred by trained immunity has been recently hypothesized to serve as a link between non-resolving vascular inflammation and atherosclerosis. Here, we provide an overview of current knowledge on trained immunity triggered by various exogenous and endogenous inducers, with particular emphasis on its pro-atherogenic effects and the underlying intracellular mechanisms that act at both the cellular level and systems level. We also discuss how trained immunity could be mechanistically linked to atherosclerosis from both preclinical and clinical perspectives. This review details the mechanisms underlying the induction of trained immunity by different stimuli, and highlights that the intracellular training programs can be different, though partly overlapping, depending on the stimulus and the biological system. Thus, clinical investigation of risk factor specific innate immune memory is necessary for future use of trained immunity-based therapy in atherosclerosis. Copyright © 2020 Zhong, Yang, Feng and Yu.Today, vaccinologists have come to understand that the hallmark of any protective immune response is the antigen. However, it is not the whole antigen that dictates the immune response, but rather the various parts comprising the whole that are capable of influencing immunogenicity. Protein-based antigens hold particular importance within this structural approach to understanding immunity because, though different molecules can serve as antigens, only proteins are capable of inducing both cellular and humoral immunity. This fact, coupled with the versatility and customizability of proteins when considering vaccine design applications, makes protein-based vaccines (PBVs) one of today's most promising technologies for artificially inducing immunity. In this review, we follow the development of PBV technologies through time and discuss the antigen-specific receptors that are most critical to any immune response pattern recognition receptors, B cell receptors, and T cell receptors. Knowledge of these receptors and their ligands has become exceptionally valuable in the field of vaccinology, where today it is possible to make drastic modifications to PBV structure, from primary to quaternary, in order to promote recognition of target epitopes, potentiate vaccine immunogenicity, and prevent antigen-associated complications.
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