CD68 Antibody Clone: GR021 Concentrate
- Known as:
- CD68 Antibody Clone: GR021 Concentrate
- Catalog number:
- 61-0184-5
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genemed
- Gene target:
- CD68 Antibody Clone: GR021 Concentrate
Related genes to: CD68 Antibody Clone: GR021 Concentrate
- 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: CD68 Antibody Clone: GR021 Concentrate
Related articles to: CD68 Antibody Clone: GR021 Concentrate
- Renal interstitial fibrosis is a key pathological feature associated with the progression of chronic kidney disease (CKD) progression. Macrophages play a central role in renal inflammation and fibrosis, and the S100 calcium binding protein A8/A9 (S100A8/A9) protein that they express participates in the immune response as an important regulatory inflammatory factor. Therefore, this study aimed to investigate the role of S100A8/A9 in M2-driven macrophage-to-myofibroblast transition (MMT) during progressive fibrosis in patients with CKD. We analyzed renal biopsy tissues from patients with CKD, constructed S100A9 overexpression and macrophage-specific knockdown mouse models, and developed an in vitro transforming growth factor β1 (TGF-β1)-induced MMT cell model. Our results revealed that S100A8/A9 was significantly upregulated in fibrotic kidneys and was mainly expressed in CD68/F4/80 macrophages with an MMT phenotype. Further experiments demonstrated that S100A9 knockdown significantly reduced renal interstitial fibrosis, collagen deposition, and tissue damage in mice with unilateral ureteral obstruction (UUO), and inhibited MMT. Conversely, S100A9 overexpression exacerbated the fibrotic phenotype. Moreover, both in vitro and in vivo, knockdown of S100A9 or pharmacological inhibition with the S100A8/A9 inhibitor paquinimod blocked the activation of the toll-like receptor 4 (TLR4)/ myeloid differentiation primary response gene 88 (MyD88)/ nuclear factor kappa-B (NF-κB) signaling pathway, reduced M2 macrophage polarization, and attenuated MMT. These findings suggest that S100A8/A9 may drives M2 macrophage-mediated MMT via the TLR4/NF-κB pathway, thereby promoting renal fibrosis. Therefore, targeting S100A8/A9 may represent a promising approach for the treatment of renal fibrosis in CKD. - Source: PubMed
Publication date: 2026/04/16
Chen XulongZha WeiweiShen JiangwenLi LinFu YanfangTian PuXunZheng BingxuanLi Cheng - Neonatal mice achieve scar-free healing after spinal cord injury (SCI) by restoring microglial homeostasis, unlike adults, where persistent microglial dyshomeostasis drives scar expansion through mechanisms that remain elusive. Using RNA sequencing, we identified protein arginine methyltransferase 6 (PRMT6) as a key regulator of this disparity, upregulated in activated microglia at adult SCI lesions but maintained at low levels in neonatal microglia after injury. In adult mice, Prmt6 deficiency restored microglial homeostasis, evidenced by increased P2Y12/TMEM119 and reduced CD68, while reducing scar formation and enhancing axonal regrowth and motor recovery. Microglia-specific Prmt6 knockdown or PRMT6 inhibitor administration recapitulated these effects. Mechanistically, PRMT6 deposits H3R2me2a at the Ppargc1a promoter to repress peroxisome proliferator-activated receptor-γ coactivator-1α（PGC-1α）, thereby inhibiting fatty acid oxidation (FAO) and disrupting microglial homeostasis. Loss of Prmt6 alleviates this epigenetic repression, restoring FAO and microglial homeostasis. These findings establish PRMT6 as a novel epigenetic regulator linking microglial dyshomeostasis and metabolic dysfunction to maladaptive scar formation in adult SCI, highlighting PRMT6 inhibition as a promising therapeutic strategy to reprogram microglial metabolism and promote neural repair. - Source: PubMed
Publication date: 2026/04/17
Peng WeilinWu ZhengqiangXiong YuGao ZhongyaLiu YishanWang ZiyiWang HaibinHan ChaofengChu WenxiangLu Xuhua - Sweet syndrome (SS) is a rare, acute, febrile neutrophilic dermatosis marked by neutrophilic infiltration into the skin, blood, and various organ systems. It manifests as painful skin eruptions, which can range from violaceous papules and plaques to vesicles and ulcers, accompanied by peripheral blood neutrophilia and fever. Sweet syndrome has three subtypes: classical, drug-induced, and malignancy-associated. There are different clinical and pathological variants of SS. However, rare variants, such as necrotizing SS and histiocytoid SS, can complicate the clinical and pathological picture, particularly in the context of hematologic malignancies. We report a case of a female patient in her late 50s with acute myeloid leukemia (AML) who developed rapidly progressing, painful, necrotic skin lesions. Clinically, the presentation raised immediate suspicion for necrotizing fasciitis. However, histopathological examination revealed a dense dermal infiltrate of mononuclear cells resembling histiocytes. Immunohistochemical staining confirmed these cells were immature myeloid precursors (MPO+/CD68+), consistent with histiocytoid SS. Despite the clinical appearance of full-thickness necrosis, the patient responded dramatically to high-dose systemic corticosteroids, avoiding the need for extensive surgical debridement. This case highlights the rare overlap of necrotizing and histiocytoid variants of SS as a paraneoplastic phenomenon in AML. It underscores the importance of recognizing these atypical presentations to prevent misdiagnosis of infection and to ensure the timely initiation of immunosuppressive therapy. Clinicians should remain vigilant, as these variants may serve as a sentinel marker for underlying or relapsed leukemia. - Source: PubMed
Publication date: 2026/03/12
Al Rawahi AyaAl-Qutaiti ZamzamAlfarsi Maimouna - Breast carcinoma with osteoclast-like stromal giant cells (OCGC) is a rare histological variant of invasive breast carcinoma. While it typically presents as a unilateral disease, its clinicopathological significance and the mechanisms underlying its formation remain incompletely understood. To our knowledge, a case of synchronous bilateral primary invasive ductal carcinoma with OCGCs has not been previously reported. A 44-year-old premenopausal woman was diagnosed with synchronous bilateral invasive ductal carcinoma with OCGCs. Imaging revealed small masses in both breasts, and core needle biopsies demonstrated invasive carcinoma with associated non-invasive components and numerous OCGCs in the tumor stroma. Both tumors were hormone receptor-positive and human epidermal growth factor receptor 2 (HER2)-negative (luminal A-like). The patient underwent bilateral mastectomy and sentinel lymph node biopsy, which showed no lymph node metastasis. The postoperative course was uneventful, and the patient has remained recurrence-free for six months after surgery. Notably, final pathological examination confirmed independent ductal carcinoma in situ (DCIS) components with OCGCs in both breasts, supporting the diagnosis of bilateral primary tumors rather than metastatic disease. Immunohistochemically, the OCGCs were CD68-positive, confirming their macrophage lineage. Genetic testing showed no pathogenic variants. This report highlights an extremely rare, pathologically confirmed case of synchronous bilateral primary breast carcinoma with OCGCs. The presence of OCGCs in both invasive and in situ components suggests that their formation can be induced at early stages of tumor development, likely reflecting a distinct immune-reactive tumor microenvironment driven by host-related factors. - Source: PubMed
Publication date: 2026/03/16
Tezuka HinakoMatsui AkiraMurata YuyaOdani ErinaTsukiyama EmiSato MarikaSasahara ManamiSeki HirohitoKinoshita Takayuki - Erdheim-Chester disease (ECD) is a rare histiocytic disorder characterized by the infiltration of tissues with foamy, xanthomatous CD68/CD163-positive, CD1a-negative histiocytosis. Pediatric ECD with chorioretinal involvement is exceedingly rare. Clinical manifestations and ophthalmic imaging findings are atypical, leading to misdiagnosis or missed diagnosis. From an ophthalmological perspective, we share an extremely rare case of pediatric ECD with chorioretinal and central nervous system infiltration, highlighting the diagnostic challenges and expanding the phenotypic spectrum of intraocular manifestations. - Source: PubMed
Publication date: 2026/04/01
Zhong HongyuLiang LicongLu Fang