Ask about this productRelated genes to: CD68 antibody
- 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
Related articles to: CD68 antibody
- Perinatal opioid exposure often compromises offspring executive function, affects offspring neuroimmune outcomes, and can impair neonatal striatal acetylcholine transmission. Therefore, we sought to examine the impact on prefrontal cortical (PFC) neurotransmission and determine whether adolescent dietary choline supplementation attenuates the effects of perinatal opioid exposure in male offspring. Using a mouse model, we found that perinatal morphine exposure reduced acetylcholine (33%) and choline (49%) in the PFC of male offspring in early adulthood, while leaving the striatum largely unaffected. Adolescent choline supplementation partially restored cholinergic deficits. While morphine exposure did not induce executive function deficits, choline supplementation improved attentional accuracy in the 5-choice serial reaction time task and reduced breakpoint in progressive ratio testing. Choline supplementation did not prevent increases in thigmotaxis after morphine exposure in male offspring. Perinatal morphine exposure increased expression of neuroinflammatory genes Apoe and Cd68 in the male basolateral amygdala, effects that were attenuated by choline supplementation. Together, these findings reveal defined neurochemical and molecular vulnerabilities to perinatal opioid exposure that may be mitigated by dietary choline supplementation. Choline supplementation was beneficial for executive function but did not specifically target morphine-induced behavioral changes. Importantly, this work is relevant for males and future work will assess female offspring. - Source: PubMed
Publication date: 2026/05/07
Sirois ChenMakela Anna GRomanova Elena VReichelt MindyCosby Kyle LGibson KaralineBochenek GraceHamilton AndrewSweedler Jonathan VSmith Brittany L - Immune cells are vital to regeneration and repair processes in the nervous system. We previously reported that myeloid cells play a critical role in nerve regeneration and locomotor recovery after peripheral nerve injury (PNI) by facilitating the clearance of inhibitory myelin debris, promoting angiogenesis, and producing neurotrophins (NTs) such as nerve growth factor (NGF), brain-derived neurotrophic factor, NT-3 and NT-4/5. Here, we show that NTs are synthesized by various types of myeloid cells after PNI, including neutrophils, macrophages and dendritic cells. Notably, we found that within the first week of PNI in male and female mice, monocyte-derived Cd11bCd68Ly6BLy6C macrophages infiltrate the sciatic nerve in an interleukin (IL)-1-dependent but CCR2-independent manner, and then locally produce mature NGF. Accordingly, depletion of circulating monocytes using PLX73086, a CSF1R inhibitor unable to cross blood-nervous system barriers, reduced NGF mRNA levels in the sciatic nerve distal stump. When polarized toward a proinflammatory phenotype , mouse macrophages rapidly release the cleaved form of NGF. Further analysis revealed that systemic administration of an anti-NGF neutralizing antibody reduced mechanical pain in mice with PNI. Together with our previous work, these results suggest that infiltrating monocyte-derived macrophages release NGF, thereby promoting both peripheral nerve regeneration and pain following injury. We unveil a pivotal role for nerve growth factor (NGF) in the modulation of pain following peripheral nerve injury (PNI). Our comprehensive investigation traces augmented NGF mRNA and protein levels during the initial week post-PNI, pinpointing the involvement of macrophages with a distinct immunophenotypic signature in NGF production. Strategic depletion experiments demonstrate monocyte-derived macrophage production of NGF in the nerve distal stump. Cultured macrophages, when polarized toward a proinflammatory phenotype, release mature NGF. Moreover, systemic NGF neutralization alleviates pain sensitivity post-PNI. This research identifies key molecular intricacies governing NGF expression and release by inflammatory macrophages, offering promising targets for therapeutics in pain management and peripheral nerve regeneration after injury. - Source: PubMed
Publication date: 2026/05/07
Kusik MaximeParé AlexandreDa Gama Monteiro FelipeNadeau SylvainFerry JuliettePineau IsabelleLessard MartineFortin NadiaVallières NicolasKerr BradleyLacroix Steve - Multicentric reticulohistiocytosis (MRH) is a rare non-Langerhans cell histiocytosis characterised by erosive arthritis and papulonodular skin lesions, frequently associated with autoimmune features. Therapeutic strategies remain empirical despite the potentially severe and disabling course. We report three cases of MRH with heterogeneous systemic involvement, all showing sustained, multidomain responses to Janus kinase (JAK) inhibitors.All patients developed inflammatory arthritis, ranging from arthralgia to destructive arthropathy, and early cutaneous papules predominantly affecting the face and trunk. Systemic manifestations included digital microangiopathy with a scleroderma-like capillaroscopic pattern in one patient and interstitial lung disease with lymphocytic alveolitis in another. Two patients fulfilled criteria for Sjögren's syndrome, and all were positive for anti-Sjögren's-syndrome-related antigen A/Ro52kD antibodies, highlighting the autoimmune overlap of MRH.Diagnosis was confirmed histologically by CD68-positive histiocytic and multinucleated giant cell infiltration. Conventional synthetic disease-modifying antirheumatic drugs and tumour necrosis factor inhibitors were ineffective or poorly tolerated, whereas tofacitinib and upadacitinib induced rapid and durable improvement across articular, cutaneous, vascular and pulmonary domains. These observations support a role for JAK-STAT signalling in MRH and suggest JAK inhibition as a rational therapeutic option in refractory multisystem disease. - Source: PubMed
Publication date: 2026/05/07
Hilliquin StéphaneDupin NicolasFranck NathalieLaurent-Roussel SaraLarousserie FrédériqueAvouac JérômeMiceli-Richard Corinne - The purpose of this study was to compare the effects of riboflavin-ultraviolet A (RF/UVA) cross-linking (CXL) and rose bengal-green light (RB/green light) CXL on corneal neovascularization (CNV) in rat eyes. - Source: PubMed
Oral MerveDayanir DuyguArik Erol Gökce NurÖzmen Mehmet Cüneyt - Tumor necrosis factor (TNF) is a key pro-inflammatory cytokine involved in various pulmonary diseases, including idiopathic pulmonary fibrosis (IPF), where it contributes to immune cell recruitment, tissue remodeling, and disease progression. Despite the therapeutic potential of TNF-targeting strategies, the lack of non-invasive tools to assess TNF activity in the lungs limits personalized treatment and trial stratification. This study aimed to evaluate the novel Affibody molecule-based positron emission tomography (PET) tracer [Ga]Z, targeting TNF, for its ability to detect inflammation in vivo using the bleomycin (BLM)-induced lung injury model in rats. - Source: PubMed
Publication date: 2026/04/28
Wegrzyniak OliviaHan HuayiEriksson Olof