CD86 Antibody
- Known as:
- CD86 Antibody
- Catalog number:
- 32223
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- CD86 Antibody
Related genes to: CD86 Antibody
- 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: CD86 Antibody
Related articles to: CD86 Antibody
- Amyotrophic lateral sclerosis (ALS) is a neurodegenerative condition that involves the targeted degeneration of motor neurons. The precise pathogenetic mechanisms are still largely unclear. In this study, we utilized the SOD1-G93A mouse model of ALS to investigate the effects of folic acid (FA), an important factor involved in homocysteine metabolism. Our results indicated that a little FA prolong the lifespan of the SOD1-G93A mice and medium and high dose FA significantly shortened the lifespan of the SOD1-G93A mice. Furthermore, we observed that overdose FA significantly elevated inflammation levels in the cerebellum, as evidenced by increased concentrations of tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), Cluster of Differentiation 68 (CD68), Cluster of Differentiation 86 (CD86), and Monocyte Chemoattractant Protein-1 (MCP-1), facilitating microglial activation. The low dose FA were the opposite of the overdose FA. Additionally, high dose FA increased the levels of phosphorylated p65 (p-p65)/p65, thereby promoting the NF-κB signaling pathway. Conversely, high dose FA inhibited the expression of total superoxide dismutase (T-SOD) while increasing the level of malondialdehyde (MDA) in the cerebellum; these effects were not observed in muscle tissue. Moreover, high dose FA elevated the levels of Bax2/Bcl-2. Concurrently, high dose FA induced increased apoptosis in SOD1-G93A mice, as demonstrated by TUNEL staining. Notably, the brain iron content of SOD1-G93A mice remained unchanged following FA treatment. These findings provide evidence that overdose FA supplementation may exert pro-inflammatory effects by promoting the NF-κB pathway, oxidative stress, and apoptosis in the context of ALS. - Source: PubMed
Publication date: 2026/09/06
Zhu YanboZhang YalunYan TaotaoLi YongboDu HaikuanZhang ShuangZhang TongheZhou Wei - Synovial plasma cell infiltration predicts inadequate response to adalimumab in patients with rheumatoid arthritis (RA), yet the cellular and molecular mechanisms underlying this association remain unclear. This study aimed to dissect the functional heterogeneity of synovial plasma cells between adalimumab responders and non-responders at single-cell resolution, and to identify the molecular pathways driving treatment resistance. - Source: PubMed
Publication date: 2026/09/04
Li JianbinJiang HouhuiWu DengfengXiong ZhenfangPeng YilinZhao JunLiu PengchengWu Rui - To investigate the therapeutic effect of Kushen Tongguan Pill (KSTG) on benign prostatic hyperplasia (BPH) induced by castration combined with testosterone propionate in rats, and to explore its underlying mechanism associated with the Toll-like receptor 4/nuclear factor κB (TLR4/NF-κB) signaling pathway. - Source: PubMed
Publication date: 2026/09/04
Chen ShaofengWang JieFeng YuhongLi ChunxuWang FuMiao LinLi YaojunLei YangyangGeng QiangLi ZhongZhao FengSun YuanDu Lijian - Insomnia is closely associated with neuroinflammation, yet the therapeutic mechanism of electroacupuncture (EA) remains unclear. This animal study investigated whether EA attenuates hypothalamic neuroinflammation in para-chlorophenylalanine (PCPA)-induced insomnia rats by suppressing the TLR4/MyD88/NF-κB p65 pathway and M1 microglial activation, using TAK-242 (HY-11109), a selective TLR4 inhibitor, as a positive control. - Source: PubMed
Publication date: 2026/08/30
Zhang MengLiu LianTan TianHe LijuanHu BingqingLi SixianJiang MengyaDeng PengRen Qingjia - IntroductionTumour-associated macrophages (TAMs) are highly plastic immune cells that polarize into tumour killing M1-like or tumour promoting M2-like macrophages depending on signals in the tumour microenvironment (TME). Exercise training may induce TAMs towards M1-like phenotypes to slow cancer progression and metastasis. In this study, we explored the effects of wheel running in tumour-challenged mice by analysing immune cell expression in metastatic tissues.MethodsArchival breast cancer lung metastases tissues of old BALB/c mice were subjected to multiplex immunofluorescence (mIHC) to quantify immune cell subsets. The immune cell expressions were then analysed against the primary mammary tumour mass, metastatic lung tissue area, as well as distance ran before and after tumour implant for the exercise mice.ResultsBased on the mIHC results from control (n=9) and exercise (n=10) mice tissues, wheel running did not significantly alter immune cell expressions relative to lung metastases or mammary tumour. Correlations between immune cell expression and the metastatic foci area revealed significant trends. Of note, F4/80 CD163 or M2-like macrophage expression is positively correlated for both control (r=0.835, =0.005) and exercise (r=0.669, =0.034). The F4/80 cells or overall macrophage expression was only positively correlated in the control (r=0.764, =0.017) group. Likewise, the mammary tumour mass was positively correlated in the control group (r=0.834, =0.010) but not in the exercise group. Interestingly, F4/80 CD86 or M1-like macrophage cells (r=0.758, =0.011) and M1/M2 ratio (r=0.642, =0.045) were only significantly correlated with mean distances ran after tumour implant.ConclusionVoluntary wheel running may shift the expression of metastatic TAMs towards anti-tumour M1-like macrophages in a dose-dependent manner after tumour challenge. This study demonstrates the importance and potential of implementing exercise training in combination with immunotherapy to treat metastatic breast cancer. - Source: PubMed
Publication date: 2026/09/04
Sitjar Patrick Henry SebastianChong Li YenLadiges WarrenYeong Joe Poh ShengGoh Jorming