Rat Anti-Mouse CD86, FITC-labeled
- Known as:
- Rat Antibody toMouse CD86, fluorecein-labeled
- Catalog number:
- 128-10056-2
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rat Anti-Mouse CD86 FITC-labeled
Related genes to: Rat Anti-Mouse CD86, FITC-labeled
- Gene:
- CD86 NIH gene
- Name:
- CD86 molecule
- Previous symbol:
- CD28LG2
- Synonyms:
- B7.2, B7-2
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-07
- Date modifiied:
- 2016-10-05
Related products to: Rat Anti-Mouse CD86, FITC-labeled
Related articles to: Rat Anti-Mouse CD86, FITC-labeled
- Macrophage-keratinocyte crosstalk is an important component of cutaneous inflammatory responses. Psoriasis is a chronic inflammatory skin disease characterized by dysregulated keratinocyte proliferation and immune dysfunction. While macrophage pro-inflammatory activation is known to exacerbate psoriatic inflammation, the underlying molecular mechanisms remain incompletely understood. TRIM28, a multifunctional regulatory protein, may play a role in this process, but whether TRIM28 regulates macrophage-keratinocyte crosstalk in a psoriasis-relevant inflammatory context remains unclear. The present study was designed as an in vitro mechanistic investigation and does not establish TRIM28 dysregulation in human psoriasis. Therefore, psoriasis is discussed only as a potential disease context, rather than as a conclusion directly supported by the present data. - Source: PubMed
Gao ZheZhang XinWang JuanYang Ni - Rheumatoid arthritis (RA) is characterized by synovial inflammation, synovial fibroblast (SF) activation, and joint destruction. Activated SFs acquire proliferative and invasive properties and interact with macrophages to maintain the inflammatory microenvironment. However, endogenous factors regulating fibroblast activation and fibroblast-macrophage communication in RA are not fully understood. In this study, we examined the expression of insulin-like growth factor binding protein 5 (IGFBP5) in RA synovium at single-cell resolution and investigated its role in SF activation and macrophage polarization. - Source: PubMed
Publication date: 2026/08/26
Bao LunminWang DaomingWang PingLi XiaoduoZhang HailongWan XiufangYuan RuiXie NanziShi MengtingWu ShuchiYue LongfeiCao Xian'eDai HaibingZheng TingJiang Hongmei - Chronically activated T-effector (Teff) cells can play a pivotal role in T-cell-mediated diseases including systemic lupus erythematosus subsets, lupus nephritis and graft-vs-host disease (GvHD). Since T cells require diverse costimulation signals to fully activate, proliferate, and differentiate into Teffs, we hypothesized that modulating two costimulatory pathways (CD28 and OX40) with a single bifunctional molecule would provide better control of pathogenic Teffs in autoimmune diseases than currently available T-cell costimulation modulators. We assessed the effects of dual-pathway blockade by M5542, a novel CD80, CD86, and OX40L antagonist and bifunctional fusion molecule. We determined the advantages of M5542 blocking both CD28 and OX40 pathways over single-pathway blockade in potency and studies, to more effectively curb T-cell-mediated inflammation in autoimmune diseases. - Source: PubMed
Publication date: 2026/08/26
Downing MichelleChristiaansen AllisonZhang LingRoe KatherineKumar NamitaDeshpande AditeeZhang HongTarcic OhadToister-Achituv MiraSoloviev MariaGross Alec WChen GangSun Chia Chi - Recently, explorations are being undertaken involving chemo-immunotherapy based on targeting cancer cells and tumor-associated macrophages (TAMs). However, these strategies mainly focus on delivering TAM modulators and chemotherapy simultaneously, without considering the effect of chemotherapy on TAMs and which may compromise TAM-modulatory action. This necessitates investigations involving sequential treatment wherein pretreatment would enable efficient M2-to-M1 repolarization before administration of chemotherapy. In this study, mannose-targeted liposomes encapsulating resiquimod (M-LIPO-RES) and doxorubicin (M-LIPO-DOX) were developed to target M2-type TAMs and cancer cells, respectively. The formulations (M-LIPO-RES and M-LIPO-DOX) were characterized for particle size, zeta potential, surface chemistry, morphology, drug entrapment efficiency, release profile, and hemolysis potential. The results showed that mannose-targeted liposomes possess a marked increase in cellular uptake in M2-polarized macrophages and MDA-MB-231 cells, revealing their potential for receptor-mediated cellular internalization. M-LIPO-RES-mediated macrophage polarization from the M2 to M1 phenotype was confirmed by analysis of the cytokine profile and estimation of TAM-associated surface proteins (e.g., CD206 and CD86), both in vitro and in vivo. The biodistribution study indicated the preferential accumulation of the developed formulation at the tumor site following intravenous administration. Furthermore, the anticancer effect was studied in the immunocompetent 4T1 mouse model, which indicated improved anticancer effect after sequential treatment (M-LIPO-RES followed by M-LIPO-DOX). Additionally, cardiac markers (i.e., troponin and CK-MB) were decreased in the targeted formulation group as compared to other treated groups, indicating a favorable cardiac safety profile. The presented targeted nano strategy preserves the immune-modulatory effect and reveals great potential for immuno-chemo response in triple-negative breast cancer (TNBC) therapy. - Source: PubMed
Publication date: 2026/09/10
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Publication date: 2026/09/09
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