Ovine MHC
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB24757 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:There is increasing recognition of the prognostic significance of tumor cell major histocompatibility complex (MHC) class II expression in anti-cancer immunity. Relapse of acute myeloid leukemia (AML) following allogeneic stem cell transplantation (alloSCT) has recently been linked to MHC class II silencing in leukemic blasts; however, the regulation of MHC class II expression remains incompletely understood. Utilizing unbiased CRISPR-Cas9 screens, we identify that the C-terminal binding protein (CtBP) complex transcriptionally represses MHC class II pathway genes, while the E3 ubiquitin ligase complex component FBXO11 mediates degradation of CIITA, the principal transcription factor regulating MHC class II expression. Targeting these repressive mechanisms selectively induces MHC class II upregulation across a range of AML cell lines. Functionally, MHC class II+ leukemic blasts stimulate antigen-dependent CD4+ T cell activation and potent anti-tumor immune responses, providing fundamental insights into the graft-versus-leukemia effect. These findings establish the rationale for therapeutic strategies aimed at restoring tumor-specific MHC class II expression to salvage AML relapse post-alloSCT and also potentially to enhance immunotherapy outcomes in non-myeloid malignancies.
2022-10-02 | GSE189771 | GEO
Project description:We previously reported that a synthetic Nod1 ligand, FK565, induced coronary arteritis in mice similar to Kawasaki disease. However, the molecular mechanisms underlying this site-specific inflammation have remained elusive. In this study, we found that CD11c+MHC class II+ cells accumulated in the heart of FK565-treated mice prior to arteritis development. We used microarray analysis to detail gene expression of CD11c+MHC class II+ cells. To obtain gene expression profile of CD11c+MHC class II+ cells, we isolated these cells from hearts of FK565-treated mice. Briefly, female mice at 8weeks age were administered 500 μg of FK565 subcutaneously at day 0 and day 3. At day6, murine hearts were removed and digested with collagenase. CD11c+MHC II+ cells were sorted as PI–CD45+Ly6G–NK1.1–CD11b+CD11c+MHC II+ using FACS Aria cell sorter (BD Biosciences). Sorted cells were subjected to RNA preparation. Two independent replicates from ten mice were made.
2015-03-31 | E-GEOD-60506 | biostudies-arrayexpress
Project description:Large scale transcriptional analysis of MHC class I haplotype diversity in sheep
| PRJEB55926 | ENA
Project description:There is increasing recognition of the prognostic significance of tumor cell major histocompatibility complex (MHC) class II expression in anti-cancer immunity. Relapse of acute myeloid leukemia (AML) following allogeneic stem cell transplantation (alloSCT) has recently been linked to MHC class II silencing in leukemic blasts; however, the regulation of MHC class II expression remains incompletely understood. Utilizing unbiased CRISPR-Cas9 screens, we identify that the C-terminal binding protein (CtBP) complex transcriptionally represses MHC class II pathway genes, while the E3 ubiquitin ligase complex component FBXO11 mediates degradation of CIITA, the principal transcription factor regulating MHC class II expression. Targeting these repressive mechanisms selectively induces MHC class II upregulation across a range of AML cell lines. Functionally, MHC class II+ leukemic blasts stimulate antigen-dependent CD4+ T cell activation and potent anti-tumor immune responses, providing fundamental insights into the graft-versus-leukemia effect. These findings establish the rationale for therapeutic strategies aimed at restoring tumor-specific MHC class II expression to salvage AML relapse post-alloSCT and also potentially to enhance immunotherapy outcomes in non-myeloid malignancies.
2022-10-02 | GSE189772 | GEO
Project description:There is increasing recognition of the prognostic significance of tumor cell major histocompatibility complex (MHC) class II expression in anti-cancer immunity. Relapse of acute myeloid leukemia (AML) following allogeneic stem cell transplantation (alloSCT) has recently been linked to MHC class II silencing in leukemic blasts; however, the regulation of MHC class II expression remains incompletely understood. Utilizing unbiased CRISPR-Cas9 screens, we identify that the C-terminal binding protein (CtBP) complex transcriptionally represses MHC class II pathway genes, while the E3 ubiquitin ligase complex component FBXO11 mediates degradation of CIITA, the principal transcription factor regulating MHC class II expression. Targeting these repressive mechanisms selectively induces MHC class II upregulation across a range of AML cell lines. Functionally, MHC class II+ leukemic blasts stimulate antigen-dependent CD4+ T cell activation and potent anti-tumor immune responses, providing fundamental insights into the graft-versus-leukemia effect. These findings establish the rationale for therapeutic strategies aimed at restoring tumor-specific MHC class II expression to salvage AML relapse post-alloSCT and also potentially to enhance immunotherapy outcomes in non-myeloid malignancies.
2022-10-02 | GSE189767 | GEO
Project description:Sequencing and annotation of equine MHC class II region
| PRJEB15527 | ENA
Project description:There is increasing recognition of the prognostic significance of tumor cell major histocompatibility complex (MHC) class II expression in anti-cancer immunity. Relapse of acute myeloid leukemia (AML) following allogeneic stem cell transplantation (alloSCT) has recently been linked to MHC class II silencing in leukemic blasts; however, the regulation of MHC class II expression remains incompletely understood. Utilizing unbiased CRISPR-Cas9 screens, we identify that the C-terminal binding protein (CtBP) complex transcriptionally represses MHC class II pathway genes, while the E3 ubiquitin ligase complex component FBXO11 mediates degradation of CIITA, the principal transcription factor regulating MHC class II expression. Targeting these repressive mechanisms selectively induces MHC class II upregulation across a range of AML cell lines. Functionally, MHC class II+ leukemic blasts stimulate antigen-dependent CD4+ T cell activation and potent anti-tumor immune responses, providing fundamental insights into the graft-versus-leukemia effect. These findings establish the rationale for therapeutic strategies aimed at restoring tumor-specific MHC class II expression to salvage AML relapse post-alloSCT and also potentially to enhance immunotherapy outcomes in non-myeloid malignancies.
2022-10-02 | GSE189769 | GEO
Project description:Metastatic progression depends upon the ability of disseminated tumor cells to evade immune surveillance. MHC-mediated antigen presentation facilitates T cell-dependent eradication of metastatic tumor cells. We identified nuclear corepressor 2 (NCOR2) as an epigenetic regulator of MHC class I molecule presentation on breast tumor cells. Patients with triple negative breast cancers (TNBC) that expressed high levels of NCOR2 also exhibited reduced metastasis-free survival and decreased MHC class I expression, and metastatic lesions in patients with TNBC had high nuclear NCOR2 and reduced CD8+ T cells. Reducing NCOR2 expression or preventing its interaction with HDAC3 enhanced innate immune cell recruitment and activity, and elevated MHC class I levels on disseminated cancer cells to potentiate CD8+ T cell activity and apoptosis induction that prevented metastatic progression. The studies provide evidence to support NCOR2 as a targetable epigenetic regulator of metastasis towards which therapies could be developed to reduce patient mortality.
2026-07-15 | GSE320158 | GEO
Project description:We previously reported that a synthetic Nod1 ligand, FK565, induced coronary arteritis in mice similar to Kawasaki disease. However, the molecular mechanisms underlying this site-specific inflammation have remained elusive. In this study, we found that CD11c+MHC class II+ cells accumulated in the heart of FK565-treated mice prior to arteritis development. We used microarray analysis to detail gene expression of CD11c+MHC class II+ cells.
2015-03-31 | GSE60506 | GEO
Project description:MHC class II alleles in Great Apes
| PRJEB27405 | ENA