Teratomas are a highly differentiated type of testicular germ cell tumors (TGCTs), the most common type of solid cancer in young men. Prominent inflammatory infiltrates are a hallmark of TGCTs, although their compositions and dynamics in teratomas remain elusive. Here, we reached out to characterize the infiltrating immune cells and their activation and polarization state by using high-throughput gene expression analysis of 129.MOLF-Chr19 mice that spontaneously develop testicular teratomas. We showed that inconspicuous testes without any apparent alterations in size or morphology can be clustered into three groups based on their expression of stemness and immune genes, supporting a model in which initial oncogenic transformation elicits a first wave of T-cell infiltration. Moderately and severely enlarged tumorous testes then displayed a progressive infiltration with T cells, monocytes/macrophages, and B cells. Importantly, T cells seem to adopt an inactive state caused by an overexpression of immune checkpoint molecules and the polarization of monocytes/macrophages to an anti-inflammatory phenotype. Our findings are supported by the analysis of metabolic gene expression, which unveiled alterations indicative of tumor growth and immune cell infiltration. Collectively, testicular teratomas, at least in mice, are characterized by a diverse inflammatory infiltrate containing T cells that putatively become inactivated, allowing the tumors to further grow. We believe that these findings may provide a rationale for the development of new immunomodulatory therapies for TGCTs.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11640870 | PMC |
J Neurochem
January 2025
Department of Oral Physiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Different taste cells express unique cell-type markers, enabling researchers to distinguish them and study their functional differentiation. Using single-cell RNA-Seq of taste cells in mouse fungiform papillae, we found that Cellular Communication Network Factor 3 (Ccn3) was highly expressed in Type III taste cells but not in Type II taste cells. Ccn3 is a protein-coding gene involved in various biological processes, such as cell proliferation, angiogenesis, tumorigenesis, and wound healing.
View Article and Find Full Text PDFMicrobiol Immunol
December 2024
Department of Oral Microbiology and Immunology, Showa University Graduate School of Dentistry, Shinagawa-ku, Tokyo, Japan.
J Physiol
December 2024
Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
Knee osteoarthritis contributes substantially to worldwide disability. Post-traumatic osteoarthritis (PTOA) develops secondary to joint injury, such as ligament rupture, and there is increasing evidence suggesting a key role for inflammation in the aetiology of PTOA and associated functional deficits. Colony stimulating factor 1 receptor (CSF1-R) has been implicated in the pathogenesis of musculoskeletal degeneration following anterior cruciate ligament (ACL) injury.
View Article and Find Full Text PDFHum Genomics
December 2024
Precision Medicine Center, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Background: Atherosclerosis (AS) is a major cause of cardiovascular diseases and neutrophil extracellular traps (NETs) may be actively involved in the development of atherosclerosis. Identifying key biomarkers in this process is essential for developing targeted treatments for AS.
Methods: We performed bioinformatics analysis using a NETosis-related gene (NRGs) set and three AS datasets (GSE100927, GSE21545, and GSE159677).
Acta Neuropathol Commun
December 2024
Department of Physiology & Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH, 44106, USA.
Mitochondrial dysfunction and α-synuclein (αSyn) aggregation are key contributors to Parkinson's Disease (PD). While genetic and environmental risk factors, including mutations in mitochondrial-associated genes, are implicated in PD, the precise mechanisms linking mitochondrial defects to αSyn pathology remain incompletely understood, hindering the development of effective therapeutic interventions. Here, we identify the loss of branched chain ketoacid dehydrogenase kinase (BCKDK) as a mitochondrial risk factor that exacerbates αSyn pathology by disrupting Complex I function.
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