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http://dx.doi.org/10.3389/frtra.2024.1519975 | DOI Listing |
Cell Rep
July 2020
Evergrande Center for Immunologic Diseases and Ann Romney Center for Neurologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA. Electronic address:
Tim-1, a phosphatidylserine receptor expressed on B cells, induces interleukin 10 (IL-10) production by sensing apoptotic cells. Here we show that mice with B cell-specific Tim-1 deletion develop tissue inflammation in multiple organs including spontaneous paralysis with inflammation in the central nervous system (CNS). Transcriptomic analysis demonstrates that besides IL-10, Tim-1 B cells also differentially express a number of co-inhibitory checkpoint receptors including TIGIT.
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March 2019
Renal Unit, Guy's and St Thomas' NHS Foundation Trust, Great Maze Pond, London SE1 9RT, United Kingdom. Electronic address:
Background: Acute T-cell mediated rejection (TCMR) is usually indicated by alteration in serum-creatinine measurements when considerable transplant damage has already occurred. There is, therefore, a need for non-invasive early detection of immune signals that would precede the onset of rejection, prior to transplant damage.
Methods: We examined the RT-qPCR expression of 22 literature-based genes in peripheral blood samples from 248 patients in the Kidney Allograft Immune Biomarkers of Rejection Episodes (KALIBRE) study.
Front Immunol
September 2019
Department of Medicine, Harvard Medical School and the Transplant Institute at Beth Israel Deaconess Medical Center, Boston, MA, United States.
Pediatr Diabetes
August 2018
Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Objective: To determine the safety and pharmacokinetics of alpha-1 antitrypsin (AAT) in adults and children.
Research Design And Methods: Short-term AAT treatment restores euglycemia in the non-obese mouse model of type 1 diabetes. A phase I multicenter study in 16 subjects with new-onset type 1 diabetes studied the safety and pharmacokinetics of Aralast NP (AAT).
Nat Commun
October 2017
Transplantation Research Center, Renal Division, Brigham and Women's Hospital and Harvard Medical School, 221 Longwood Avenue, Boston, MA, 02115, USA.
Phosphatidylinositol-3-kinases (PI3K) γ and δ are preferentially enriched in leukocytes, and defects in these signaling pathways have been shown to impair T cell activation. The effects of PI3Kγ and PI3Kδ on alloimmunity remain underexplored. Here, we show that both PI3Kγ and PI3Kδ mice receiving heart allografts have suppression of alloreactive T effector cells and delayed acute rejection.
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