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
- Repetitive low-level blast exposures in rats induce the development of a post-traumatic stress disorder (PTSD)-like phenotype and evolving chronic brain vascular alterations. These alterations included atherogenic-like lesions characterized by increased extravasation of blood elements into the arterial subendothelial layers, nuclear expression of c-Fos in endothelial and vascular smooth muscle cells, vascular hyperplasia, foam cell formation, and ultimately vascular rupture. Foam cells were mainly of macrophage/microglial or of vascular smooth muscle cell origin with upregulated expression of MHC II and of its co-stimulatory molecule CD86, which is characteristic of antigen-presenting cells. Foam cells also upregulated the lysosomal CD68 marker, indicating macrophage/microglial phagocytic and inflammatory activity. Foam cells of vascular smooth muscle cell origin were present at arteriolar bends, kinks, and bifurcations and were associated with a progressive arterial network degeneration in regions with enlarged perivascular spaces. Foam cell inclusions also contained the gelatinase MMP-9, which is involved in extracellular matrix degradation, and the pro-inflammatory cytokine TNF-α that further induces foam cell formation. These findings indicate that the chronic atherogenic lesions associated with blast-induced vascular degeneration may trigger a progressive pro-inflammatory state and expand the progressive vascular degeneration associated with the PTSD-like phenotype. - Source: PubMed
Publication date: 2026/04/23
Gama Sosa Miguel ADe Gasperi RitaLind Rachel HPryor DylanPerez Gissel MPerez Garcia Georgina SAbutarboush RaniaKawoos UsmahZhu Carolyn WJanssen William G MHof Patrick RAhlers Stephen TElder Gregory A - The purpose of this study was to explore the effect of ubiquitin-specific protease (USP) 22 overexpression on spinal cord injury (SCI) in rats and its potential mechanism, to assess its role in the recovery of neurological function. - Source: PubMed
Yu Ming-ChenLi Xiao-LinLu Shuai-JinNing Ming-LiangYan ZhenzhongYang Yadong - Cytomegalovirus (CMV) infection has been associated with an increased risk of tuberculosis, but the underlying mechanisms remain unclear. Here, we used the murine CMV (MCMV), a virus genetically and biologically related to human CMV, to interrogate potential mechanisms. MCMV-infected macrophages showed reduced expression of CD80, CD86, and MHC class II, decreased phagocytosis of mycobacteria, and enhanced mycobacterial killing compared with MCMV-uninfected macrophages. Splenocytes from MCMV-infected mice better controlled mycobacterial growth than those from MCMV-uninfected mice. However mice infected with MCMV and subsequently challenged intranasally with mycobacteria were not more susceptible to mycobacterial infection , irrespective of the tested MCMV infection route, the interval between infections, or Bacillus Calmette-Guérin (BCG) vaccination status. These findings offer insights into how prior CMV infection may modulate host responses to mycobacteria. Further studies using more virulent mycobacterial strains, more susceptible mouse models, and varied infection timings are needed to extend these results. - Source: PubMed
Publication date: 2026/03/27
Li ShuailinHutchings ClaireKorompis MarcellusDe Voss ChristopherAteere AlbertaSatti ImanKlenerman PaulMcShane HelenStylianou Elena - Depression remains a major global health challenge. Microglial polarization imbalance and subsequent neuroinflammation are core pathological mechanisms. Given current treatment limitations, developing natural products with fewer side effects is a critical research priority. - Source: PubMed
Publication date: 2026/04/15
Guo MeiCui CanZheng Zhou-JuanLi NaYuan Hai-ShengChen Yu-HanDing HuaZhang YeCheng YongPiao Xiang-Lan - Damage-Associated Molecular Patterns (DAMPs) or alarmins are endogenous molecules that activate immune cells and drive an inflammatory response. Derangements in DAMP levels are associated with pregnancy disorders. Our previous study demonstrated that an excess of High Mobility Group Box 1 (HMGB1), an alarmin, in the uterine cavity leads to implantation failure in rats. The present study investigated whether HMGB1-induced implantation failure was associated with perturbations in the uterine immune microenvironment. Recombinant HMGB1 with/without its inhibitor glycyrrhizin was administered on day 3 post-coitum (p.c.) in Wistar rats. Uterine fluid, uterine horns, and lymph nodes were collected on day 5 p.c. HMGB1-associated implantation failure was found to be associated with altered proportions of uNK cells, Tregs; altered phenotype of macrophages, and impaired decidualization. While total CD68+ macrophage proportion did not change significantly, the proportion of M2 macrophages (CD68+CD163+) was reduced at the implantation sites in the HMGB1-treated uterine horns. The proportion of activated M2 macrophages (CD68+CD163+CD86+MHCIIlow) was also reduced in the HMGB1-treated animals. This was accompanied by a significant increase in IL-1β and IL-5 cytokine levels in the uterine fluid. Further, our studies demonstrated that some of these effects, such as a decrease in the uNK cell proportion and modulation in the macrophage phenotype, result from the direct effect of excess HMGB1 on the endometrium. These effects were not observed in animals receiving both HMGB1 and glycyrrhizin. Thus, an excess of HMGB1 in the uterine cavity alters the proportion/phenotype of uterine immune cells and thereby compromises the implantation competence of the endometrium. - Source: PubMed
Publication date: 2026/04/21
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