9 to 16.8). The strength of evidence was low quality because of imprecision and indirectness. The subgroup analyses revealed that the sample size influenced on estimated injury prevalence and methodological quality influenced on estimated incidence. Injuries were more prevalent in the shoulder, for non-ambulant para athletes, and in the lower limbs, for ambulant para athletes. Para athletes show high prevalence and incidence of musculoskeletal injuries. Current very low-quality and low-quality evidence suggests that future high-quality studies with systematic data collection, larger sample size and specificities of para athletes are likely to change estimates of injury prevalence and incidence in para athletes. CRD42020147982.CRD42020147982.Foxo1 is an essential transcription factor required for the survival and differentiation of memory CD8 T cells, yet it is unclear whether these Foxo1-dependent functions are inherently coupled. To address this question, we examined the effects of different Foxo1 posttranslational modifications. Phosphorylation of Foxo1 by Akt kinases at three distinct residues is well characterized to inhibit Foxo1 transcriptional activity. However, the effect of Foxo1 phosphorylation within its DNA-binding domain at serine 209 by Mst1 kinase is not fully understood. In this study, we show that an S209A phospho-null Foxo1 exhibited Akt-dependent nuclear trafficking in mouse CD8 T cells and augmented the expression of canonical Foxo1 target genes such as Il7r and Sell In contrast, an S209D phosphomimetic Foxo1 (SD-Foxo1) was largely excluded from the nucleus of CD8 T cells and failed to transactivate these genes. RNA sequencing analysis revealed that SD-Foxo1 was associated with a distinct Foxo1-dependent transcriptional profile, including genes mediating CD8 effector function and cell survival. Despite defective transactivation of canonical target genes, SD-Foxo1 promoted IL-15-mediated CD8 T cell survival in vitro and survival of short-lived effector cells in vivo in response to Listeria monocytogenes infection. However, SD-Foxo1 actively repressed CD127 expression and failed to generate memory precursors and long-lived memory T cells. Together, these data indicate that S209 is a critical residue for the regulation of Foxo1 subcellular localization and for balancing CD8 T cell differentiation and survival.Invariant NKT (iNKT) cells are an innate-like population characterized by their recognition of glycolipid Ags and rapid cytokine production upon activation. Unlike conventional T cells, which require TCR ligation, iNKT cells can also be stimulated independently of their TCR. This feature allows iNKT cells to respond even in the absence of glycolipid Ags, for example, during viral infections. Although the TCR-dependent and -independent activation of iNKT cells have been relatively well established, the exact contributions of IL-12, IL-18, and TLRs remain unclear for these two activation pathways. check details To definitively investigate how these components affect the direct and indirect stimulation of iNKT cells, we used mice deficient for either MyD88 or the IL-12Rβ2 in the T cell lineage. Using these tools, we demonstrate that IL-12, IL-18, and TLRs are completely dispensable for the TCR activation pathway when a strong agonist is used. In contrast, during murine CMV infection, when the TCR is not engaged, IL-12 signaling is essential, and TLR signaling is expendable. Importantly, to our knowledge, we discovered an intrinsic requirement for IL-18 signaling by splenic iNKT cells but not liver iNKT cells, suggesting that there might be diversity, even within the NKT1 population.High-dimensional cytometry is a powerful technique for deciphering the immunopathological factors common to multiple individuals. However, rational comparisons of multiple batches of experiments performed on different occasions or at different sites are challenging because of batch effects. In this study, we describe the integration of multibatch cytometry datasets (iMUBAC), a flexible, scalable, and robust computational framework for unsupervised cell-type identification across multiple batches of high-dimensional cytometry datasets, even without technical replicates. After overlaying cells from multiple healthy controls across batches, iMUBAC learns batch-specific cell-type classification boundaries and identifies aberrant immunophenotypes in patient samples from multiple batches in a unified manner. We illustrate unbiased and streamlined immunophenotyping using both public and in-house mass cytometry and spectral flow cytometry datasets. The method is available as the R package iMUBAC (https//github.com/casanova-lab/iMUBAC).With ever-improving methods of cell characterization, the field of immunology has enjoyed unprecedented opportunities to resolve distinctions between lymphocyte populations. However, this has led to a proliferation of "subset" designations that threatens to complicate and confuse clear identification of populations that share critical functional traits. This article discusses some of the challenges associated with a uniform approach to assigning subset designations to memory T-cell populations.The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a β-coronavirus, is the causative agent of the COVID-19 pandemic. Like for other coronaviruses, its particles are composed of four structural proteins Spike (S), Envelope (E), Membrane (M) and Nucleoprotein (N) proteins. The involvement of each of these proteins and their interactions are critical for assembly and production of β-coronavirus particles. Here, we sought to characterize the interplay of SARS-CoV-2 structural proteins during the viral assembly process. By combining biochemical and imaging assays in infected vs. transfected cells, we show that E and M regulate intracellular trafficking of S as well as its intracellular processing. Indeed, the imaging data reveal that S is re-localized at endoplasmic reticulum (ER)-Golgi intermediate compartment (ERGIC) or Golgi compartments upon co-expression of E or M, as observed in SARS-CoV-2-infected cells, which prevents syncytia formation. We show that a C-terminal retrieval motif in the cytoplasmic tail of S is required for its M-mediated retention in the ERGIC, whereas E induces S retention by modulating the cell secretory pathway.