Immunization of mice with irradiated (20 Gy) or non-irradiated allogeneic spleen cells i.v. induces delayed-type hypersensitivity (DTH)-reactive T cells, as well as suppressor T cells, against histocompatibility antigens. The suppressor T cells are unable to suppress the induction and functional activity of the simultaneously activated DTH-reactive T cells. However, the suppressor T cells do suppress the generation of DTH-reactive T cells after subsequent s.c. immunization of the same mice, and after transfer into secondary recipients. Systemic transfer of suppressor T cells is effective the first few days after their induction, and affects the afferent limb of the DTH response. The population of suppressor T cells, which is essential for the systemic transfer of suppression, appeared to be Lyt-1+2+. Splenectomy experiments showed that the spleen is not essential for induction of the suppressor T cells. The precursors of the suppressor T cells belong to the pool of recirculating T lymphocytes; they are insensitive to adult thymectomy and can be depleted by antithymocyte serum treatment.
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http://dx.doi.org/10.1097/00007890-198405000-00014 | DOI Listing |
Int J Nanomedicine
January 2025
School of Basic Medicine, Ningxia Medical University, Yinchuan, People's Republic of China.
Background: Colorectal cancer (CRC) is a highly malignant and aggressive gastrointestinal tumor. Due to its weak immunogenicity and limited immune, cell infiltration lead to ineffective clinical outcomes. Therefore, to improve the current prophylaxis and treatment scheme, offering a favorable strategy efficient against CRC is urgently needed.
View Article and Find Full Text PDFClin Transl Radiat Oncol
March 2025
Department of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, the Netherlands.
Background And Purpose: Understanding the cellular and molecular effect of proton radiation, particularly the increased DNA damage complexity at the distal end of the Bragg curve, is current topic of investigation. This work aims to study clonogenic survival and DNA damage foci kinetics of a head and neck squamous cell carcinoma cell line at various positions along a double passively scattered Bragg curve. Complementary studies are conducted to gain insights into the link between cell survival variations, experimentally yielded foci and the number and complexity of double strand breaks (DSBs).
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Leonard Davis School of Gerontology, University of Southern California, Los Angeles, California, USA.
Introduction: Iron-mediated cell death (ferroptosis) is a proposed mechanism of Alzheimer's disease (AD) pathology. While iron is essential for basic biological functions, its reactivity generates oxidants which contribute to cell damage and death.
Methods: To further resolve mechanisms of iron-mediated toxicity in AD, we analyzed post mortem human brain and ApoEFAD mice.
Mol Cancer
January 2025
Department of Radiation Oncology, Peking University Third Hospital, Beijing, 100191, China.
Background: Sorafenib, an FDA-approved drug for advanced hepatocellular carcinoma (HCC), faces resistance issues, partly due to myeloid-derived suppressor cells (MDSCs) that enhance immunosuppression in the tumor microenvironment (TME).
Methods: Various murine HCC cell lines and MDSCs were used in a series of in vitro and in vivo experiments. These included subcutaneous tumor models, cell viability assays, flow cytometry, immunohistochemistry, and RNA sequencing.
EMBO J
January 2025
Department of Geriatrics, Gerontology Institute of Anhui Province, Centre for Leading Medicine and Advanced Technologies of IHM, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
mTOR plays a pivotal role in cancer growth control upon amino acid response. Recently, CDK inhibitor P27KIP1 has been reported as a noncanonical inhibitor of mTOR signaling in MEFs, via unclear mechanisms. Here, we find that P27KIP1 degradation via E3 ligase TRIM21 is inhibited by human micropeptide hSPAR through its C-terminus (hSPAR-C), causing P27KIP1's cytoplasmic accumulation in breast cancer cells.
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