4 results match your criteria: "Newcastle University Translational and Clinical Research Institute and NIHR Newcastle Biomedical Research Centre[Affiliation]"
Human CARMIL2 deficiency underlies a broader immunological and clinical phenotype than CD28 deficiency.
J Exp Med
February 2023
Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM, Necker Hospital for Sick Children, Paris, France.
Article Synopsis
- Patients with inherited CARMIL2 or CD28 deficiencies show defective T cell signaling, but CARMIL2's role is less understood.
- Research indicates that the mutant CARMIL2 alleles affect T cell activation and lead to specific immunological issues including low counts of memory T cells and NK cells, as well as weak antibody responses.
- CARMIL2 deficiency leads to serious health issues by age 10, including frequent infections and inflammation, and milder symptoms are observed in patients with somatic reversions in T cells.
Loss of T cell tolerance in the skin following immunopathology is linked to failed restoration of the dermal niche by recruited macrophages.
Cell Rep
May 2022
Department of Haematology, University College London (UCL) Cancer Institute, London WC1E 6DD, UK; Institute for Immunity and Transplantation, Division of Infection and Immunity, University College London, London NW3 2PF, UK. Electronic address:
Article Synopsis
- T cell pathology in the skin causes an influx of monocytes, but we lack knowledge about how these recruited cells behave over time and affect immune balance in the skin.
- Research combining a mouse model of acute graft-versus-host disease (aGVHD) and patient samples reveals that disease leads to the differentiation of macrophages specifically in the skin's dermis and results in a dominance of these macrophages, reducing the presence of resting MHCII cells.
- After the disease resolves, exposing the altered skin to certain substances can cause overactivation of regulatory T cells (Tregs), leading to a loss of immune tolerance and an enduring impact on immune regulation, referred to as an "immunological scar."
GATA2 deficiency phenotype associated with tandem duplication of GATA2 and overexpression of GATA2-AS1.
Blood Adv
December 2021
Newcastle University Translational and Clinical Research Institute and NIHR Newcastle Biomedical Research Centre, Newcastle upon Tyne, United Kingdom.
A 3-year-old girl of nonconsanguineous healthy parents presented with cervical and mediastinal lymphadenopathy due to Mycobacterium fortuitum infection. Routine blood analysis showed normal hemoglobin, neutrophils, and platelets but profound mononuclear cell deficiency (monocytes < 0.1 × 109/L; B cells 78/μL; NK cells 48/μL).
View Article and Find Full Text PDFFLT3 ligand in acute myeloid leukemia: a simple test with deep implications.
Leuk Lymphoma
February 2021
Newcastle University Translational and Clinical Research Institute and NIHR Newcastle Biomedical Research Centre, Newcastle University, Newcastle Upon Tyne, UK.
In contrast to Fms-like tyrosine kinase 3 (FLT3), the influence of FLT3 ligand (FLT3L) on acute myeloid leukemia (AML) biology and disease prognosis has been poorly described. Here we provide an overview of the role played by FLT3L in AML. While being a cytokine implicated in the regulation of hematopoiesis, both in normal situation and after intensive chemotherapy, FLT3L has also a role in enhancing proliferation, inhibiting apoptosis and conferring resistance to FLT3 inhibitors in AML.
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