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http://dx.doi.org/10.1111/bjh.18655 | DOI Listing |
Proc Natl Acad Sci U S A
November 2024
BIO5 Institute, University of Arizona, Tucson, AZ 85719.
Viruses with broad tissue distribution and cell tropism successfully replicate in various nutrient environments in the body. Several viruses reprogram metabolism for viral replication. However, many studies focus on metabolic reprogramming in nutrient-rich conditions that do not recapitulate physiological environments in the body.
View Article and Find Full Text PDFJ Clin Invest
November 2024
Children's Health and Discovery Initiative.
Human cytomegalovirus (HCMV) profoundly impacts host T and NK cells across the lifespan, yet how this common congenital infection modulates developing fetal immune cell compartments remains underexplored. Using cord blood from neonates with and without congenital HCMV (cCMV) infection, we identify an expansion of Fcγ receptor III-expressing (FcγRIII-expressing) CD8+ T cells following HCMV exposure in utero. Most FcγRIII+CD8+ T cells express the canonical αβ T cell receptor (TCR), but a proportion express noncanonical γδ TCR.
View Article and Find Full Text PDFJ Immunol
October 2024
Department of Immunobiology, University of Arizona College of Medicine-Tucson, Tucson, AZ.
CMV drives the accumulation of virus-specific, highly differentiated CD8 memory T cells (memory inflation [MI]). In mice, MI was shown to directly correlate with the CMV infection dose, yet the CMV-associated CD8 MI plateaus over time. It is unclear how MI is regulated with aging.
View Article and Find Full Text PDFElife
June 2024
Institute of Virology, Medical Center University of Freiburg, Freiburg, Germany.
Human leucocyte antigen class I (HLA-I) molecules play a central role for both NK and T-cell responses that prevent serious human cytomegalovirus (HCMV) disease. To create opportunities for viral spread, several HCMV-encoded immunoevasins employ diverse strategies to target HLA-I. Among these, the glycoprotein US10 is so far insufficiently studied.
View Article and Find Full Text PDFCell Mol Immunol
August 2024
Molecular Signaling and Cell Death Unit, VIB-UGent Center for Inflammation Research, Flanders Institute for Biotechnology, Ghent, Belgium.
Acute systemic inflammation critically alters the function of the immune system, often promoting myelopoiesis at the expense of lymphopoiesis. In the thymus, systemic inflammation results in acute thymic atrophy and, consequently, impaired T-lymphopoiesis. The mechanism by which systemic inflammation impacts the thymus beyond suppressing T-cell development is still unclear.
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