Pulmonary surface active material (SAM), purified from canine lung lavage fluids, is a phospholipid-rich lipoprotein with potent immunosuppressive activity. Experiments were performed to identify those components of SAM that were responsible for this immunosuppressive effect. Results indicated that the lipid, and not the protein, fraction of SAM was immunosuppressive. Two phospholipids, phosphatidylglycerol and phosphatidylcholine, were identified as the predominant immunosuppressive components of the SAM-lipid fraction. lymphocyte proliferation in response to mitogenic or allogeneic stimulation was suppressed by intact SAM, SAM-lipid, phosphatidylglycerol, and phosphatidylcholine. Each of these preparations inhibited RNA, protein and DNA synthesis by mitogen-stimulated lymphocytes. Antioxidants consistently failed to diminish the immunosuppressive properties of SAM or its lipid components. The mechanism of this immunosuppressive action of SAM and its phospholipid components remains undefined. Our data indicate, however, that it is unlikely to be due either to cytotoxicity or to an artifact of lipid oxidation in vitro.
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J Clin Invest
January 2025
Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality worldwide, with inflammation playing a pivotal role in its pathogenesis. T lymphocytes are crucial components of the adaptive immune system that have emerged as key mediators in both cardiac health and the development and progression of CVD. This Review explores the diverse roles of T cell subsets, including Th1, Th17, γδ T cells, and Tregs, in myocardial inflammatory processes such as autoimmune myocarditis and myocardial infarction.
View Article and Find Full Text PDFThe lung tumor microenvironment is composed of various cell types, including cancer cells, stromal and immune cells, as well as extracellular matrix (ECM). These cells and surrounding ECM create a stiff, hypoxic, acidic, and immunosuppressive microenvironment that can augment the resistance of lung tumors to different forms of cell death and facilitate invasion and metastasis. This environment can induce chemo/radiotherapy resistance by inducing anti-apoptosis mediators such as phosphoinositide 3-kinase (PI3K)/Akt, signal transducer and activator of transcription 3 (STAT3), and nuclear factor of κB (NF-κB), leading to the exhaustion of antitumor immunity and further resistance to chemo/radiotherapy.
View Article and Find Full Text PDFRespir Res
January 2025
Department of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
H3 lysine 4 trimethylation (H3K4me3) modification and related regulators extensively regulate various crucial transcriptional courses in health and disease. However, the regulatory relationship between H3K4me3 modification and anti-tumor immunity has not been fully elucidated. We identified 72 independent prognostic genes of lung adenocarcinoma (LUAD) whose transcriptional expression were closely correlated with known 27 H3K4me3 regulators.
View Article and Find Full Text PDFCell Commun Signal
January 2025
Digestive Disease Center, The First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang Province, 154000, China.
Background: Programmed cell death ligand 1 (PD-L1) expression on immune cells is correlated with the efficacy of immune checkpoint inhibitor (ICI) therapy in various types of cancer. Platelets are important components of the tumour microenvironment (TME) and are widely involved in the development of many types of cancer including colorectal cancer (CRC). However, the role of PD-L1 positive platelets in ICI therapy for CRC remains unknown.
View Article and Find Full Text PDFAnn Surg Oncol
January 2025
Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Background: Tumor microvasculature is an important component of the tumor microenvironment (TME), and it has been reported that tumor microvasculature induces TME to become immunosuppressive via vascular endothelial growth factor. However, the significance of this in adenocarcinoma with epidermal growth factor receptor (EGFR) common mutations has not been fully investigated.
Methods: We analyzed 262 patients with adenocarcinoma harboring EGFR common mutations who underwent surgery at Kyushu University Hospital between 2006 and 2021.
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