T-cell activation is a characteristic of organ rejection. T cells, located in the draining lymph nodes of the transplant recipient, are faced with non-self-molecules presented by antigen presenting cells and become activated. Activated T cells are characterized by up-regulated surface antigens, such as costimulatory molecules, adhesion molecules, chemokine receptors, and major histocompatibility complex class II molecules. Surface antigen expression can be followed by flow cytometry using monoclonal antibodies in either cell function assays using donor-specific or nonspecific stimulation of isolated cells or whole blood and without stimulation on circulating lymphocytes. Molecules such as CD30 can be proteolytically cleaved off the surface of activated cells in vivo, and the determination of the soluble protein (sCD30) in serum or plasma is performed by immunoassays. As promising biomarkers for rejection and long-term transplant outcome, CD28 (costimulatory receptor for CD80 and CD86), CD154 (CD40 ligand), and sCD30 (tumor necrosis factor receptor superfamily, member 8) have been identified. Whereas cell function assays are time-consuming laboratory-developed tests which are difficult to standardize, commercial assays are frequently available for soluble proteins. Therefore, more data from clinical trials have been published for sCD30 compared with the surface antigens on activated T cells. This short review summarizes the association between selected surface antigens and immunosuppression, and rejection in solid organ transplantation.
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http://dx.doi.org/10.1097/FTD.0000000000000259 | DOI Listing |
Sci Rep
January 2025
College of Animal Science and Technology, Ningxia Key Laboratory of Ruminant Molecular and Cellular Breeding, Ningxia University, Yinchuan, 750021, China.
Currently, the identification of valuable candidate genes affecting milk fat synthesis in dairy cows is still limited, and the specific regulatory mechanism is still unknown. In this study, we used primary bovine mammary epithelial cells(BMECs)as a model and utilized overexpression and knockdown techniques for the PI4K2A gene to investigate the specific mechanisms by which it regulates lipid metabolism in BMECs. We studied whether PI4K2A regulates the inhibition of trans-10, cis-12 conjugated linoleic acid (t10,c12-CLA) on lipid synthesis in BMECs.
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January 2025
Department of Gastroenterology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710014, Shaanxi Province, China.
The role of human epidermal growth factor 2 (HER2) in male breast cancer (MBC) is poorly defined. A comprehensive description of HER2 status was conducted. A total of 6,015 MBC patients from 45 studies and 135 MBC patients with sequencing data were identified.
View Article and Find Full Text PDFNPJ Vaccines
January 2025
Jiangzhong Cancer Research Center, Jiangxi University of Chinese Medicine, Nanchang, Jiangxi, China.
Tumor-derived exosomes (TDEs) mediate oncogenic communication, which modifies target cells to reinforce a tumor-promoting microenvironment. TDEs support cancer progression by suppressing anti-tumor immune responses, promoting metastasis, and conferring drug resistance. Thus, targeting TDEs could improve the efficacy of anti-cancer treatments and control metastasis.
View Article and Find Full Text PDFJ Pathol Clin Res
January 2025
State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers and National Clinical Research Center for Digestive Diseases, Xijing Hospital of Digestive Diseases, Fourth Military Medical University, Xi'an, PR China.
CXC chemokine receptor 4 (CXCR4) and programmed cell death-ligand 1 (PD-L1) are two critical molecules involved in the tumor immune microenvironment. However, the impact of platinum drugs, such as cisplatin, on CXCR4 or PD-L1 expression and the underlying mechanisms in gastric cancer (GC) remain unknown. Moreover, the correlation between their expression levels in GC remains elusive.
View Article and Find Full Text PDFJ Immunother Cancer
January 2025
Division of Infection, Immunity and Respiratory Medicine, The University of Manchester, Manchester, UK
Background: Programmed cell death 1 (PD-1) signaling blockade by immune checkpoint inhibitors (ICI) effectively restores immune surveillance to treat melanoma. However, chronic interferon-gamma (IFNγ)-induced immune homeostatic responses in melanoma cells contribute to immune evasion and acquired resistance to ICI. Poly ADP ribosyl polymerase 14 (PARP14), an IFNγ-responsive gene product, partially mediates IFNγ-driven resistance.
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