CIITA polyclonal antibody
- Known as:
- CIITA pab (anti-)
- Catalog number:
- PAB9942
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CIITA polyclonal antibody
Related genes to: CIITA polyclonal antibody
- Gene:
- CIITA NIH gene
- Name:
- class II major histocompatibility complex transactivator
- Previous symbol:
- MHC2TA
- Synonyms:
- C2TA, NLRA
- Chromosome:
- 16p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-12
- Date modifiied:
- 2019-04-23
Related products to: CIITA polyclonal antibody
Related articles to: CIITA polyclonal antibody
- In human melanoma, tumor cell-specific MHC class II expression is associated with improved response to programmed death 1 and programmed death-ligand 1 blockade; yet the direct effect of melanoma cell-specific MHC class II expression on anti-melanoma T cell responses remains largely unknown. In the clinically relevant Yale University Mouse Melanoma Exposed to Radiation (YUMMER) cell lines, MHC class II expression was IFN-γ-inducible in a subset of cells. Transduction of melanoma cells with CIITA resulted in uniformly high, constitutive expression of MHC class II. YUMMER.G cells transduced with CIITA vector had increased in vivo tumor growth in wild-type mice compared to melanoma cells transduced with empty vector. YUMMER.G cells transduced with empty or CIITA vectors had the same in vivo tumor growth in RAG-/- mice, indicating that the difference in tumor growth between CIITA- and empty-transduced cells was dependent on an intact adaptive immune system. CIITA-transduced YUMMER.G tumors exhibited an increased frequency and infiltration depth of CD4+ T cells, an increased frequency of T regulatory cells, and a decreased frequency and infiltration depth of CD8+ T cells, compared to empty-transduced tumors. Antibody depletion revealed that CIITA- and empty-transduced YUMMER.G tumors were constrained by CD4+ and CD8+ T cells, but only tumor growth of CIITA-transduced cells was decreased by CD25 blockade, which primarily blocks T regulatory cell function. Overall, this work reveals a potential pro-tumorigenic role of melanoma cell-specific overexpression of MHC class II. - Source: PubMed
Macy Anne MHerrmann Lauren MThornley Erin MAdams Anngela CStoll Carly RLancaster Jessica NHastings Karen Taraszka - Obesity is increasingly implicated in hematopoietic malignancies, yet its role in mutation-driven myeloid leukemias remains unclear. Using UK Biobank data from over 440,000 individuals, we found obesity traits including elevated BMI and waist-to-hip ratio were associated with type 2 diabetes, increased plasma IL-17A (interleukin-17A), reduced GLP-1R (glucagon like peptide 1 receptor) expression, and heightened risk of myeloid malignancies. Transplantation of protein tyrosine phosphatase non-receptor type 11, PTPN11 (Shp2E76K/+) mutant hematopoietic stem/progenitors into obese mice demonstrated that metabolic inflammation accelerates leukemogenesis via myeloid cell expansion, lipid metabolic rewiring, IL-17A activation, and accumulation of M2-like tumor-associated macrophages (TAMs), accompanied by T-cell exhaustion and impaired antigen presentation. Notably, dual therapy with an anti-IL-17A antibody and a GLP-1R agonist reversed these effects, by reducing M2-like TAMs, restoring Ciita-dependent antigen presentation, Tyk2-mediated IFNγ signaling, reactivated T-cell responses, and reducing leukemic burden. These findings establish IL-17A driven, metabolism-coupled immunosuppression as a mechanistic link between obesity and SHP2-mutant myeloid leukemias, highlighting a tractable therapeutic strategy for high-risk obese patients. - Source: PubMed
Publication date: 2026/06/23
Kapur ReubenLi LinkeKanumuri RahulPadam Kanaka Sai RamRamdas BaskarPasala ChiranjeeviChiosis GabrielaPalam Lakshmi ReddyKumar RameshKoyama SatoshiNatarajan PradeepHaneline Laura SYu ZhiPasupuleti Santhosh Kumar - Tumors downregulate NLRC5 expression to reduce MHC-I and evade CD8 T cell-mediated killing. Introducing full-length NLRC5 (N5FL) or NLRC5-CIITA chimeric protein (N5CA) can restore tumor immunogenicity. Here, we elucidated the underlying mechanisms and also evaluated the requirement of NLRC5 expression in antigen-presenting cells (APCs) of the host for tumor control. - Source: PubMed
Publication date: 2026/06/02
Shukla AkhilMoradzad MohammadQuenum Akouavi Julite IrmineLucier Jean-FrançoisArmas Cayarga AnnyLévesque DominiqueBoisvert François-MichelKufer Thomas ARamanathan SheelaIlangumaran Subburaj - Osteoarthritis (OA) involves progressive extracellular matrix (ECM) degradation in articular cartilage. We previously revealed that the mA demethylase ALKBH5 stabilizes Runx2 mRNA in chondrocytes via YTHDF1, thereby increasing MMP and ADAMTS expression, causing ECM degradation. However, the transcriptional co-regulators of Runx2 remain unidentified. - Source: PubMed
Publication date: 2026/06/16
Nie GuanghuaLi YiZhao HongmouWang DongZhang YanYang XinquanWen Xiaodong - Primary cutaneous follicle center lymphomas (PCFCLs) are indolent B-cell neoplasms limited to the skin and effectively managed with local therapies. Distinguishing PCFCL from systemic follicular lymphoma (sFL) with cutaneous involvement (FL_CI) is challenging due to overlapping features. We performed an integrated pathological and genetic analysis of skin samples of 24 PCFCL and 10 FL_CI, which showed subtle pathological changes (decreased BCL2 and CD10, increased CD23 expression in PCFCL), but markedly distinct mutational landscapes. FL_CI exhibited recurrent mutations in chromatin-modifying genes ( 90%, 90%, and 30%), closely resembling sFL. In contrast, PCFCL displayed a more heterogeneous profile, with mutations affecting B-cell development, cell adhesion, and immune evasion. These molecular alterations identified three distinct PCFCL subgroups. Group 1 (44%) harbored mutations in immune evasion genes (, , , and ) and was associated with CD10 negativity, diffuse architecture, and localization in non-photoexposed areas. Group 2 (20%) showed activating and mutations, consistent CD23 and CD10 positivity, and exclusive presentation in sun-exposed sites. Group 3 (20%) shared a similar clinicopathological profile to Group 2 but was defined by mutations. Clonal origin and mutational evolution were studied in five patients, one with synchronous PCFCL and four with sequential samples from two PCFCL and 2 FL_CI. This analysis supports a model of PCFCL oncogenesis driven by circulating progenitors following complex evolutionary patterns, including convergent evolution and greater clonal diversity at relapse. Overall, our study refines the mechanisms driving PCFCL pathogenesis, while providing a framework for PCFCL differential diagnosis and clinical management. - Source: PubMed
Publication date: 2026/05/29
Combalia AndreaVidal-Robau NuriaNadeu FerranLópez CristinaFrigola GerardLopez-Oreja IreneGarcia NoeliaBashiri MelikaMozas PabloLopez-Guillermo ArmandoSalaverria ItziarEstrach TeresaCampo EliasGarcia-Herrera AdrianaAlbero Robert