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Background: Chronic graft-versus-host disease (cGVHD) manifests with characteristics of autoimmune disease with organs attacked by pathogenic helper T cells. Recent studies have highlighted the role of T cells in cGVHD pathogenesis. Due to limited understanding of underlying mechanisms, preventing cGVHD after allogenic hematopoietic cell transplantation (HCT) has become a major challenge.

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Purpose: We report the case of a 6-year-old boy who presented with muscular hypertonia, impaired growth, and recurrent infections, who was diagnosed with purine nucleoside phosphorylase (PNP) deficiency with two novel mutations in the gene. He underwent a hematopoietic stem cell transplantation (HSCT) from an unrelated donor, and we observed the clinical outcome.

Methods: We retrospectively analyzed the clinical manifestations and outcomes of this patient who underwent HSCT.

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Myeloid chimerism better reflects donor stem cell engraftment than whole-blood chimerism in assessing graft function following allogeneic hematopoietic stem cell transplant (HCT). We describe our experience with 130 patients aged younger than 18 years, treated with allogeneic HCT using bone marrow or PBSC from HLA-matched donors for non-malignant diseases, whose pre-transplant conditioning therapy included alemtuzumab and who were monitored with lineage-specific chimerism after transplant. At 6 years post-transplant, overall survival (OS) was 91.

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Whereas much knowledge exists on the expression of IFN pathways in the blood of people living with HIV (PLWH), its role has only recently been appreciated in the gastrointestinal tract. Thus, the aim was to evaluate the gut mRNA expression levels of innate immune genes involved in the HIV-host interaction and their association with CD4 T cell activation in long-term HAART-experienced PLWH. PLWH had increased TLR4, IFN-α2, IFN-α14, IFN-β and IFNAR1 mRNAs levels in LPLs, as well as increased frequencies of CD4 T lymphocytes expressing CD38 or HLA-DR compared to the healthy donors.

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Monoclonal antibodies enhance innate immunity, while bispecific T cell engager antibodies redirect adaptive T cell immunity. To stimulate both innate and adaptive mechanisms, we created a bifunctional eCD16A/anti-CD3-BFP adapter protein for combined use with clinically approved monoclonal IgG1 antibodies. The adaptor protein contains the extracellular domain of the human CD16A high-affinity variant, which binds the Fc domain of IgG1 antibodies, and an anti-human CD3 single-chain variable fragment that redirects T cell cytotoxicity.

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