Anti-Human CD68 FITC 100 tests
- Known as:
- Antibody toHuman CD68 fluorecein 100 tests
- Catalog number:
- 11-0689-73
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD68 FITC 100 tests
Related genes to: Anti-Human CD68 FITC 100 tests
- Gene:
- CD68 NIH gene
- Name:
- CD68 molecule
- Previous symbol:
- -
- Synonyms:
- SCARD1, macrosialin, GP110, DKFZp686M18236, LAMP4
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-11
- Date modifiied:
- 2016-10-05
Related products to: Anti-Human CD68 FITC 100 tests
Related articles to: Anti-Human CD68 FITC 100 tests
- Alcohol-associated liver disease (ALD) is the leading cause of liver-related mortality worldwide. ALD is progressive, involving chronic, non-resolving inflammation and immune dysfunction. Despite this knowledge, the mechanisms behind immune dysfunction in ALD are not well understood. Here, we characterized a recently described intracellular complement system, the "complosome", making use of explanted liver tissue from ALD patients, chronic-plus-binge feeding to anaphylatoxin receptor deficient mice, and in vitro models of macrophage activation. Expression of anaphylatoxin receptors was increased in liver explants from ALD patients compared to healthy donor liver in CD68+ macrophages. After chronic-plus-binge feeding, ethanol increased surface expression of C3aR1 and C5aR1 and intracellular C5aR1 pool on CD11bF4/80 Kupffer cells. C5aR1-/-, but not C3aR1-/- mice, were protected from binge-ethanol induced liver injury while deficiency of either receptor protected from ethanol-induced expression of pro-inflammatory cytokines and recruitment of immune cells to the liver. In BMDMs, ethanol and LPS treatment increased expression of intracellular complement components C3, C5, C3aR1, and C5aR1; anaphylatoxin receptors were co-expressed with lysosomal and mitochondrial membrane markers. LPS-induced expression of NLRP3 and production of IL-1β was attenuated in C3aR1- and C5aR1-deficient BMDMs. C3aR1/C5aR1-/- DKO mice were protected from ethanol-induced elevations in liver injury and inflammation. In conclusion, ethanol impacts macrophages by increasing intracellular complosome components that may impact non-resolving inflammation in ALD. - Source: PubMed
Publication date: 2026/05/29
Rutt Lauren NKirkpatrick Shannon MAnton Paige EWinter AndrewCapper CourtneyBurchill Matthew AFritz Kristofer SMcCullough Rebecca L - Rosai-Dorfman Disease (RDD) is a rare histiocytic disorder typically affecting lymph nodes. Extranodal RDD is uncommon, and isolated central nervous system (CNS) or spinal disease is particularly rare, limiting guidance on diagnosis and management. - Source: PubMed
Publication date: 2026/05/28
Ramesh RithvikOsorio Robert CPekmezci MelikeBoreta LaurenDatta DebajyotiAlan Nima - Pro-inflammatory cytokines, TNF and IL-1B, are essential for testicular homeostasis. Diacerein, an anti-inflammatory drug, inhibits these cytokines, impairing M2 macrophages and Leydig cells (LCs). However, its impact on Sertoli cells (SCs) and M1 (CD68) macrophages remains unknown. - Source: PubMed
Publication date: 2026/05/29
Jesus Elide Loise Freitas deSilva André Acácio Souza daAkinsomisoye Olumide StephenSilva Erick J RCerri Paulo Sérgiode Oliveira Salmo AzambujaSasso-Cerri Estela - Malakoplakia is a rare chronic granulomatous disorder predominantly occurring in immunocompromised patients, with renal parenchymal involvement being exceptionally rare, likely because of dysfunctional macrophage clearance of bacteria. Here, we report a case of a 69-year-old woman with elevated creatinine levels and bilateral kidney lesions, but no identifiable immunosuppressive factors. was isolated from urine analysis. Histopathological examination showed nearly complete replacement of renal parenchyma by 3 distinct morphological zones: a granulomatous area rich in CD68 macrophages and giant cells with eosinophilic granular cytoplasm, an inflammatory zone dominated by mixed inflammatory cells, and a collagen-dominant fibrotic zone. Numerous Michaelis-Gutmann (MG) bodies with significant size variation (maximum dimension 187 μm × 96 μm) were observed. Electron microscopy showed abnormally enlarged lysosomes containing fibrillary components, as well as crystalloid or targetoid bodies, representing different developmental stages of MG bodies. After treatment with levofloxacin and prednisone, the patient's creatinine levels improved, and renal cortical thickness normalized. This case not only demonstrates the histological features of malakoplakia at different stages but also shows the ultrastructural progression of MG bodies, suggesting that malakoplakia should be considered in the differential diagnosis of elderly patients with unexplained kidney function decline. - Source: PubMed
Publication date: 2026/04/21
Ren Ya-LiQiu De-JunLi Xin-LunWang Su-Xia - Autism spectrum disorder (ASD) encompasses a diverse range of neurodevelopmental conditions characterized by variations in social interactions, stereotyped behaviors, and sensory processing differences. Altered tactile and auditory sensory processing is among the most frequently observed phenotypes in ASD animal models, particularly in Shank3 gene knockout rodents. Previous research has focused extensively on neural activity associated with Shank3 deficiency and sensory dysregulation, but the role of glial cells, especially microglia, has been largely overlooked. Microglia, the central nervous system's primary immune cells, are crucial for regulating neural activity throughout development and adulthood. To address this gap, we used immunofluorescence microscopy to examine microglial morphology, density, and the fluorescence intensity of IBA1 and CD68 in adult Shank3 knockout and wild type mice, focusing on brain regions primarily involved in the acoustic startle circuit, while including the somatosensory cortex as a control region. We examined six brain regions involved in auditory and tactile sensory processing: the somatosensory cortex, central nucleus of the amygdala (CeA), caudal pontine reticular nucleus (PnC), reticulotegmental nucleus (RtTg), inferior colliculus(IC), and cochlear nucleus (CN). Our findings showed a 39% increase in IBA1 expression in the CeA (p = 0.01) and a 13% increase in microglial density in the PnC (p = 0.02). However, we found no evidence of robust microglial activation, as indicated by the absence of morphological changes or alterations in CD68 expression across the examined regions. These results indicate that moderate microglial alterations in the Shank3 mouse model may be circuit-dependent rather than a global phenomenon across all sensory modalities, warranting further investigation into the interplay between glial cells and sensory circuit dysfunction. - Source: PubMed
Publication date: 2026/05/18
Ren XinHavekes RobbertKas Martien J H