CTLA4_HUMAN CD152 ELISA tesk kit
- Known as:
- CTLA4_HUMAN CD152 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15797
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- CTLA4_HUMAN CD152 ELISA tesk kit
Related genes to: CTLA4_HUMAN CD152 ELISA tesk kit
- Gene:
- CTLA4 NIH gene
- Name:
- cytotoxic T-lymphocyte associated protein 4
- Previous symbol:
- CELIAC3, IDDM12
- Synonyms:
- CD152, CD, GSE, CTLA-4
- Chromosome:
- 2q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-25
- Date modifiied:
- 2019-04-23
Related products to: CTLA4_HUMAN CD152 ELISA tesk kit
Related articles to: CTLA4_HUMAN CD152 ELISA tesk kit
- Myeloid lineage-derived cells are key orchestrators of immune function and contribute to several chronic inflammatory disorders, such as rheumatoid arthritis (RA). The landscape of how these detrimental pro-inflammatory roles evolve over the course of the disease and the impact of therapies on them is being unraveled by recent immune-cell profiling studies. An alternative phenotyping using CD4 and CD45R0 expression to assess monocyte (Mo) and DC subsets allowed us to re-evaluate CD26 expression, an antigen with key migratory functions via its dipeptidyl peptidase (DPP4) activity on chemokines, in myeloid cells. Myeloid DCs barely express CD26 (while plasmacytoid pDCs do), and the intermediate Mo (intMo) subset is enriched in CD26. In a cohort of RA patients under treatment, together with the known expansion of Mo and the impairment of DC subsets and intMo, the CD26 expression was reduced, except for the intMo subset, enriched in CD26. The CD26 expression levels correlated with disease activity (DAS28 and its components), with therapy-specific patterns. Treatment with classical or biologic DMARDs, anti-IL6R, CTLA4-Ig, anti-TNF and anti-CD20, differentially modulated Mo subsets, the latter two reducing classical monocytes (cMo) while anti-TNF modestly increasing pDCs frequencies. Only anti-IL6R therapy increased total intMo % while decreasing the CD26+ intMo % (anti-CD20 also decreased the latter; on the contrary, CTLA4-Ig and anti-TNF increased it). Therapies variably restored CD26 density, except for anti-IL6R and anti-CD20. In conclusion, given that DPP4 inhibitors have shown contradictory effects in RA, their specific impact on these CD26+ APC functions warrants further investigation. Furthermore, the strong both positive and negative correlations found between soluble sCD26 levels and CD26+ frequencies (most strongly with pDCs) might support a sCD26 secretion independent of membrane-bound CD26, and CD26+ cell frequency associations with levels of anti-CD26 autoantibodies might suggest Ag-Ab complexes involvement on CD26 expression only in certain contexts. - Source: PubMed
Publication date: 2026/06/26
Kotrulev MartinViñuela Juan EPego-Reigosa José MGomez-Tourino IriaCordero Oscar J - To compare the retention rate, hazard ratio of treatment discontinuation, and effectiveness of tumor necrosis factor inhibitor (TNFi), interleukin-6 inhibitor (IL-6i), and cytotoxic T lymphocyte-associated antigen-4-Ig (CTLA4-Ig) in patients with rheumatoid arthritis (RA) and reduced kidney function. - Source: PubMed
Higuchi TomoakiTanaka EiichiInoue EisukeSugano EriSugitani NaohiroOchiai MoekoIkari KatsunoriHarigai Masayoshi - Asbestos exposure is associated with asbestos-related diseases such as pleural plaques, asbestosis, lung cancer, malignant mesothelioma (MM), as well as several other types of cancer. Although the exact mechanism underlying the development of asbestos-related diseases is not yet fully understood, the immune system may play an important role. Immune checkpoints such as programmed cell death receptor 1 (PD-1), programmed cell death ligand-1 (PD-L1), and cytotoxic T lymphocyte-associated protein 4 (CTLA-4) regulate immune responses and are crucial for maintaining immune tolerance, while defects in these mechanisms can lead to the development of cancer. The aim of present study was to investigate the association of polymorphisms in the immune checkpoint genes for PD-1 (), PD-L1 (), and CTLA-4 () with the risk of asbestos-related diseases. - Source: PubMed
Publication date: 2026/06/26
Zeljkovic IrmaGoricar KatjaBlagus TanjaFranko AlenkaKovac ViljemDolzan Vita - The clinical translation of alloantigen-specific regulatory T cells (AS-Tregs) is constrained by their low frequency in peripheral blood, limited purity, and functional instability following prolonged expansion. To address these hurdles, we developed a strategy to isolate and expand a functional CD25CD27CD70 AS-Treg population. Initially, Tregs were co-cultured with allogeneic dendritic cells in the presence of IL-15, IL-2, and retinoic acid. Proliferating CD25CD27CD70 AS-Tregs were subsequently FACS-sorted and expanded via polyclonal anti-CD3/CD28 stimulation with IL-15, IL-2, rapamycin, and TGF-β. Over three weeks, this protocol yielded a 434-fold expansion, achieving >95% purity (CD25FOXP3) while maintaining a substantial degree (>60%) of -TSDR demethylation, a hallmark of stable Treg lineage commitment. The expanded CD27 AS-Tregs exhibited a robust immunoregulatory phenotype, characterized by high expression of Helios, CTLA-4, and CD39, as well as chemokine receptors associated with allograft and lymphoid tissue homing (CXCR3, CCR4, and CCR7). Functionally, CD27 AS-Tregs suppressed T cell proliferation in an antigen-specific manner, even after exposure to inflammatory cytokines, and showed a concentration-dependent chemotactic response to CXCL10 . In addition, these cells maintained lineage fidelity by lacking the production of inflammatory cytokines such as IFN-γ and IL-17A. Accordingly, transcriptional profiling by RNA sequencing confirmed the enrichment of immunoregulatory signatures and revealed minimal changes in gene expression when expanded Tregs were exposed to inflammatory conditions. Overall, our findings suggest that CD27 AS-Tregs represent promising candidates for more stable, long-term Treg therapy to support transplant tolerance. - Source: PubMed
Publication date: 2026/06/10
Cortés-Hernández ArimelekArteaga-Cruz SaúlMartínez Iturbe Iyari IRosas-Cortina KatyaVigil Mora Marco ALegorreta-Anguiano ErickReyes Barrientos Judith EÁlvarez-Salazar Evelyn KCervera AlejandraSánchez-Hernández Beatriz EDomínguez Armando GamboaSoldevila Gloria - Hepatocellular carcinoma (HCC) is a leading global malignant tumor with poor prognosis. Immune checkpoint inhibitors (ICIs) have become a breakthrough treatment for HCC, but a systematic landscape analysis of global ICI clinical trials is lacking. - Source: PubMed
Publication date: 2026/06/10
Cao JunjieChen YanruZhang LichuanLou JunyiLi ShuangWen HaiquanHuang RongMa Lin