Rat CD4+ T cells are divided phenotypically by the anti-CD45RC monoclonal antibody OX22 into subsets with contrasting functions. Stimulation of T cells in vitro is known to induce a change in isoform from CD45RC+ to CD45RC-. We have investigated the in vitro conditions which promote a switch in isoform in the opposite direction. We observed that a majority of CD45RC- CD4 T cells (> 90%) spontaneously re-expressed CD45RC during the first 1-3 days of culture in both the presence and absence of alloantigen. The T cells remained CD45RC+ when cultured for 7 days in serum-free growth medium. However, alloantigen-activated lymphocytes, expressing the interleukin-2 receptor (IL-2R), downregulated CD45RC by day 4 and remained CD45RC- during the course of the experiment. Using mixtures of allotype-marked CD45RC+ and CD45RC- T cells, it was demonstrated that each subset showed comparable survival, IL-2R expression and time courses of activation in response to alloantigen. The repertoire of neither subset was, therefore, deficient in terms of allorecognition. The rapid re-expression of CD45RC in culture was accompanied by a change in function: CD45RC+ "converts", obtained by overnight culture of CD45RC- T cells, induced significantly higher graft-versus-host responses. Thus, the transition in culture from CD45RC- to CD45RC+ reflects a major functional reprogramming of the cell and not a trivial modulation of a surface antigen.
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http://dx.doi.org/10.1002/eji.1830230117 | DOI Listing |
iScience
December 2024
Institut NeuroMyoGène, Physiopathologie et Génétique du Neurone et du Muscle Université Claude Bernard Lyon 1, CNRS U5261, Inserm U1315, University Lyon, Lyon, France.
In Duchenne muscular dystrophy (DMD), muscle stem cells' (MuSCs) regenerative capacities are overwhelmed leading to fibrosis. Whether MuSCs have intrinsic defects or are disrupted by their environment is unclear. We investigated cell behavior and gene expression of MuSCs from DMD or healthy human muscles.
View Article and Find Full Text PDFPurpose Of Review: We aim to provide an updated perspective on the recent advancements in gene therapy for polycystic kidney disease (PKD), a genetic disorder with significant morbidity. Given the rapid evolution of gene therapy technologies and their potential for treating inherited diseases, this review explores the therapeutic prospects and challenges in applying these technologies to PKD.
Recent Findings: Significant progress has been made in understanding the genetic underpinnings of PKD, making it a prime candidate for gene therapy.
J Cell Biol
January 2025
Biochemistry, Cell and Systems Biology, Institute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, UK.
Sci Rep
October 2024
Division of Nephrology, Department of Internal Medicine, University of Michigan, 1500 E. Medical Center Drive, SPC 5364, Ann Arbor, MI, 48109, USA.
Primary cultures of proximal tubule cells are widely used to model the behavior of kidney epithelial cells in vitro. However, de-differentiation of primary cells upon culture has been observed and appreciated for decades, yet the mechanisms driving this phenomenon remain poorly understood. This confounds the interpretation of experiments using primary kidney epithelial cells and prevents their use to engineer functional kidney tissue ex vivo.
View Article and Find Full Text PDFMethods Mol Biol
July 2024
Cancer Epigenetics Group, Harry Perkins Institute of Medical Research, Perth, WA, Australia.
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