CIITA antibody - middle region (ARP37976_P050)
- Known as:
- CIITA (anti-) - middle region (ARP37976_P050)
- Catalog number:
- arp37976_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CIITA antibody - middle region (ARP37976_P050)
Related genes to: CIITA antibody - middle region (ARP37976_P050)
- 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 antibody - middle region (ARP37976_P050)
Related articles to: CIITA antibody - middle region (ARP37976_P050)
- 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 - Porcine circovirus type 2d (PCV2d) is one of the predominant genotypes associated with porcine circovirus-associated diseases, which highlights the need for effective vaccination strategies. This study assessed the expression profile of the major histocompatibility complex class II transactivator (CIITA) gene in pigs immunized with recombinant PCV2d virus-like particles (VLPs). Recombinant PCV2d capsid protein was expressed in insect cells and self-assembled into VLPs, which were further used to immunize piglets. Peripheral blood mononuclear cells were analyzed for CIITA expression by qRT-PCR and interferon-gamma (IFN γ) production by ELISA. Following PCV2d VLP immunization, CIITA expression increased over time, peaked on day 21, and was associated with elevated IFN-γ secretion. A significant positive correlation between CIITA expression and IFN γ levels was detected in pooled analyses. These findings demonstrate that PCV2d VLPs endorse Th1-biased immune responses and further enhance the CIITA-mediated antigen presentation, supporting their potential as an effective vaccine platform against PCV2d. - Source: PubMed
Publication date: 2026/06/06
Wilson Varay LDeb RajibMaity Hemanta KumarSengar Gyanendra SinghSandilya Pragya BhushanDas Pranab JyotiPegu Seema RaniRai VishalDeka Naba JyotiDas RajibRajkhowa SwarajGupta Vivek Kumar - During Mycobacterium tuberculosis (Mtb) infection, infected alveolar macrophages (AMs) initially up-regulate a nuclear factor erythroid 2-related factor 2 (NRF2)-regulated cell-protective program, which is detrimental to host control and impedes AM activation, including MHC II expression. MHC II is critical for CD4 T cell activation and host immunity during Mtb infection. We hypothesized that NRF2 regulates the MHC II pathway and AM antigen presentation to T cells. We found that NRF2 inhibits MHC II, but not MHC I, specifically in AMs, following Mtb infection in vitro and in vivo. NRF2 dampens Ciita and H2-Ab1 gene expression in uninfected AMs, and MHC II inhibition by NRF2 is retained following innate stimuli and IFNγ exposure. NRF2 expression in Mtb-infected AMs impedes their ability to activate ESAT6-specific CD4 T cells. Thus, although NRF2 expression enhances cell-protective functions, it has the unexpected consequence of limiting innate-adaptive crosstalk, which can impair CD4 T cell activation and host immunity during Mtb infection. - Source: PubMed
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