Currently, therapy for squamous cancer (SqC) is unsatisfactory. Staphylococcal enterotoxin B (SEB) has strong immune regulatory activity. This study tests the hypothesis that SEB enforces the effect of immunotherapy on SqC growth in a mouse model. C3H/HeN mice and the SqC cell line squamous cell carcinoma VII were used to create an SqC mouse model. Immune cell assessment was performed by flow cytometry. Real-time RT-PCR and western blotting were used to evaluate target molecule expression. An apoptosis assay was used to assess the suppressive effect of T helper-9 (Th9) cells on the SqC cells. The results showed that immunotherapy consisting of SEB plus SqC antigen significantly inhibited SqC growth in the mice. The frequency of Th9 cells was markedly increased in the SqC tissue and mouse spleens after treatment. SEB markedly increased the levels of signal transducer and activator of transcription 5 phosphorylation and the expression of histone deacetylase-1 (HDAC1) and PU.1 (the transcription factor of the interleukin 9 (IL-9) gene) in CD4 T cells. Exposure to SqC-specific Th9 cells markedly induced SqC cell apoptosis both in vitro and in vivo. In conclusion, the administration of SEB induces Th9 cells in SqC-bearing mice, and theseTh9 cells inhibit SqC growth.
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http://dx.doi.org/10.1038/cmi.2015.88 | DOI Listing |
Front Immunol
January 2025
Department of Pharmaceutical Sciences, Marshall University School of Pharmacy, Huntington, WV, United States.
CD4 T cell activation induces dramatic changes to cellular metabolism for supporting their growth and differentiation into effector subsets. While the cytokines IL-4, TGF-β and IL-21 promote differentiation into Th9 cells, metabolic factors regulating this process remain poorly understood. To assess the role of lipid metabolism in human Th9 cell differentiation, naïve CD4 T cells were purified from blood of healthy volunteers and cultured in the presence or absence of compounds targeting PPAR-γ, acetyl-CoA-carboxylase 1 (ACC1), and AMP-activated protein kinase (AMPK) for four days.
View Article and Find Full Text PDFJ Invest Dermatol
December 2024
Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. Electronic address:
T9 cells are implicated in allergic skin inflammation and depend on the transcription factor PPAR-γ for full effector function. In this study, we uncovered a role for PPAR-γ in the amino acid metabolism of human T9 cells. In in-vitro-primed T9 cells, PPAR-γ expression positively correlated with the expression of SLC7A8, which encodes LAT2, a transporter of large neutral amino acids, including cystine.
View Article and Find Full Text PDFClin Med Insights Oncol
December 2024
Department of Gastroenterology & Nutrition, University Hospital of North Norway, University of Tromsø, Tromsø, Norway.
Background: Inflammation is the most important deriving force for the development of colitis-associated colorectal cancer (CAC) through the Inflammation-Pretumor dysplasia-CAC sequence. T helper (Th) subsets Th9 and Th17 cells can potentially stimulate inflammation in the ulcerative colitis (UC). Therefore, Th9 and Th17 cells may play a promoting role in the colitis-associated dysplasia (CAD).
View Article and Find Full Text PDFCell Rep Med
December 2024
The Zhongzhou Laboratory for Integrative Biology, Henan Key Laboratory of Brain Targeted Bio-Nanomedicine, School of Life Sciences, Henan University, Kaifeng, Henan 475004, China; Henan-Macquarie University Joint Centre for Biomedical Innovation, School of Life Sciences, Henan University, Kaifeng, Henan 475004, China. Electronic address:
Glioblastoma (GBM) stem cells (GSCs) contribute to poor prognosis in patients with GBM. Identifying molecular markers is crucial for developing targeted therapies. Here, we identify cluster of differentiation 97 (CD97) as an optimal GSC surface antigen for potential targeting by chimeric antigen receptor (CAR) T cell therapy through in vitro antibody screening.
View Article and Find Full Text PDFJ Immunother Cancer
December 2024
Department of Orthopedics, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, People's Republic of China
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