ArticlePloS one2012
SH2D2A modulates T cell mediated protection to a B cell derived tumor in transgenic mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Bioinformatics analysis of intrinsic drivers of immune dysregulation in multiple myeloma to elucidate immune phenotypes and discover prognostic gene signatures.Scientific reports · 2025Article
- Endothelial transcriptomic, epigenomic and proteomic data challenge the proposed role for TSAd in vascular permeability.Angiogenesis · 2025Article
- Article
- Construction and Validation of a Prognostic Model Based on Pyroptosis-related Genes in Bladder Cancer.Combinatorial chemistry & high throughput screening · 2024Article
- A novel CD8Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Population genomic, olfactory, dietary, and gut microbiota analyses demonstrate the unique evolutionary trajectory of feral pigs.Molecular ecology · 2022Article
- T Cell-Specific Adaptor Protein Regulates Mitochondrial Function and CD4Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Time-Course Transcriptome Analysis of Gingiva-Derived Mesenchymal Stem Cells Reveals ThatFrontiers in cell and developmental biology · 2019Article
- Polarity of CD4+ T cells towards the antigen presenting cell is regulated by the Lck adapter TSAd.Scientific reports · 2018Article
- The mutational landscape ofOncotarget · 2018Article
- Reduced MCMV Δm157 viral clearance in the absence of TSAd.Scientific reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundT cell specific adapter protein (TSAd), encoded by the SH2D2A gene, modulates signaling downstream of the T cell receptor (TCR). Young, unchallenged SH2D2A-deficient C57BL/6 mice exhibit a relatively normal immune phenotype. To address whether SH2D2A regulates physiologic immune responses, SH2D2A-deficient TCR-transgenic BALB/c mice were generated. The transgenic TCR recognizes a myeloma-derived idiotypic (Id) peptide in the context of the major histocompatibility complex (MHC) class II molecule I-E(d), and confers T cell mediated resistance to transplanted multiple myeloma development in vivo. PRINCIPAL
findingsThe immune phenotype of SH2D2A-deficient C57BL/6 and BALB/c mice did not reveal major differences compared to the corresponding wild type mice. When challenged with myeloma cells, Id-specific TCR-transgenic BALB/c mice lacking SH2D2A displayed increased resistance towards tumor development. Tumor free TCR-transgenic SH2D2A-deficient mice had higher numbers of Id-specific single positive CD4+ thymocytes compared to TCR-transgenic wild-type mice.
conclusionOur results suggest a modulatory role for SH2D2A in T cell mediated immune surveillance of cancer. However, it remains to be established whether its effect is T-cell intrinsic. Further studies are required to determine whether targeting SH2D2A function in T cells may be a potential adjuvant in cancer immunotherapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.