Murine resting (G(0)) T lymphocytes contained no detectable mRNA of 3-phosphoglycerate dehydrogenase (PHGDH) catalyzing the first step in the phosphorylated pathway of l-serine biosynthesis. Immobilized anti-CD3 activation of G(0) T cells expressed the PHGDH mRNA in G(1) with a maximum level in S phase. G(0) T cells activated with either immobilized anti-CD3 plus CsA or PBu(2), which failed to drive the activated T cells to enter S phase, did not express the PHGDH mRNA unless exogenous rIL-2 was added. Blocking of IL-2R signaling by adding anti-IL-2 and anti-IL-2Rα resulted in no expression of the PHGDH mRNA during immobilized anti-CD3 activation of G(0) T cells. Deprivation of l-serine from culture medium or addition of antisense PHGDH oligonucleotide significantly reduced [(3)H]TdR incorporation of activated T cells. These results indicate that the PHGDH gene expression, dictated by IL-2R signaling, is a crucial event for DNA synthesis during S phase of activated T cells.
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http://dx.doi.org/10.1016/j.cellimm.2013.12.003 | DOI Listing |
Int Immunopharmacol
January 2025
AT-31 BIO Inc., 403 Business Incubation Center, Kyungpook National University, 80 Daehak-ro, Buk-gu, Daegu 41566, Republic of Korea; Laboratory of Immunobiology, School of Life Science and Biotechnology, College of Natural Sciences, Kyungpook National University, 80 Daehak-ro, Buk-gu, Daegu 41566, Republic of Korea. Electronic address:
Recombinant GH16B β-agarase-catalyzed liquefaction of 5-7 %(w/v) melted agarose at 50 °C completely hydrolyzed agarose into neoagarohexaose (NA6) and neoagarotetraose (NA4). Subsequent saccharification by recombinant GH50A β-agarase or recombinant GH50A β-agarase/recombinant GH117A α-neoagarobiose hydrolase at 35 °C converted NA6/NA4 into neoagarobiose (NA2) or 3,6-anhydro-L-galactose (L-AHG)/D-galactose, respectively. Purification of NA6/NA4 and NA2 was achieved by Sephadex G-15 column chromatography, while L-AHG was purified by Sephadex G-10, achieving ≥ 98 % purity.
View Article and Find Full Text PDFSe Pu
July 2024
Department of Chemistry, College of Science, Southern University of Science and Technology, Shenzhen 518055, China.
J Immunother Cancer
June 2024
Department of Immunology and Regenerative Biology, Weizmann Institute of Science, Rehovot, Israel
Background: Adoptive cancer immunotherapy, using engineered T-cells, expressing chimeric antigen receptor or autologous tumor infiltrating lymphocytes became, in recent years, a major therapeutic approach for diverse types of cancer. However, despite the transformative potential of adoptive cancer immunotherapy, this field still faces major challenges, manifested by the apparent decline of the cytotoxic capacity of effector CD8 T cells upon their expansion. To address these challenges, we have developed an ex vivo "synthetic immune niche" (SIN), composed of immobilized CCL21 and ICAM1, which synergistically induce an efficient expansion of antigen-specific CD8 T cells while retaining, and even enhancing their cytotoxic potency.
View Article and Find Full Text PDFCell J
October 2023
Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran.
Objective: Chimeric antigen receptor (CAR) T cell therapy has recently emerged as a promising approach for the treatment of different types of cancer. Improving CAR T cell manufacturing in terms of costs and product quality is an important concern for expanding the accessibility of this therapy. One proposed strategy for improving T cell expansion is to use genetically engineered artificial antigen presenting cells (aAPC) expressing a membrane-bound anti-CD3 for T cell activation.
View Article and Find Full Text PDFPLoS One
June 2023
Research Organization for Nano and Life Innovation, Waseda University, TWIns, Shinjuku, Tokyo, Japan.
Follicular helper T (Tfh) cells are crucial for humoral immunity. Dysregulation of Tfh cell differentiation can cause infectious, allergic, and autoimmune diseases. To elucidate the molecular mechanisms underlying Tfh cell differentiation, we attempted to establish an in vitro mouse model of Tfh cell differentiation in the absence of other cell types.
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