Ask about this productRelated genes to: CCR5 antibody
- Gene:
- CCR5 NIH gene
- Name:
- C-C motif chemokine receptor 5 (gene/pseudogene)
- Previous symbol:
- CMKBR5
- Synonyms:
- CKR-5, CC-CKR-5, CKR5, CD195, IDDM22
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1996-05-15
- Date modifiied:
- 2019-01-10
Related products to: CCR5 antibody
Related articles to: CCR5 antibody
- Trained immunity enhances innate host defense by endowing monocytes with memory-like properties, yet the underlying integrated metabolic and epigenetic mechanisms remain elusive. Here, we demonstrate that coimmunization with Bacille Calmette-Guérin (BCG) and bacterial lipoprotein (BLP) induces a durable form of trained immunity that provides robust, long-term protection against polymicrobial sepsis from early life into adulthood. Single-cell RNA sequencing revealed that this effect is mediated by an expansion of CCR5 memory-like monocytes with enhanced antimicrobial capacity. Mechanistically, BCG + BLP vaccination activated the AKT-mTOR-HIF-1α axis, driving glycolytic reprogramming and lactate accumulation. Elevated lactate enhanced KAT2B-dependent histone H3K18 lactylation, an epigenetic mark directly facilitating the transcription of phagocytic and inflammatory genes. In addition, BCG + BLP stimulation of human cord blood mononuclear cells induced CCR5 monocytes that recapitulated trained immunity features. These findings identify a lactate-KAT2B-H3K18la epigenetic axis that orchestrates the long-term reprogramming of CCR5 monocytes, highlighting CCR5 monocytes as a promising therapeutic target for modulating innate immunity against lethal sepsis. - Source: PubMed
Publication date: 2026/08/21
Xu LingqiHao WenyanYang YingyiWang YuLi YaoshuangGong YuanDing YifangHuang JieBai ZhenjiangShan QiangKang RuiWang Jiang HuaiWang HaichaoBilliar Timothy RWang JianTang DaolinZhou Huiting - People living with HIV (PLWH) exhibit a markedly elevated risk of developing atherosclerotic cardiovascular disease (ASCVD), a phenomenon not entirely attributable to conventional risk factors, thereby indicating the existence of an immune-mediated residual risk. Trained immunity may represent a critical underlying mechanism. - Source: PubMed
Publication date: 2026/08/05
Shi JinchuanZheng RongrongZhang Zhongdong - Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease characterized by excessive extracellular matrix deposition and irreversible architectural distortion of the lung. Fibrotic remodeling is driven by dynamic interactions among endothelial, fibroblast, epithelial and immune cells. Although pulmonary endothelial cells (ECs) are increasingly recognized as important contributors to IPF pathogenesis, the molecular and cellular events underlying endothelial dysfunction remains poorly understood. Using integrative multi-omics analyses of human IPF lungs combined with functional in vitro assays, we identify ACKR1-expressing venous endothelial cells (ACKR1+ VECs) as critical regulators of a pathogenic niche that promotes lung fibrosis. Single-cell RNA sequencing and spatial transcriptomics analyses reveal that ACKR1+ VECs exhibit a distinct pro-fibrotic and pro-inflammatory transcriptional program enriched for hypoxia responses, extracellular matrix remodeling, and immune cell recruitment. In both mouse and human fibrotic lungs, ACKR1+ VECs localize adjacent to fibroblastic foci and are surrounded by pro-fibrotic CD68+/CCR5+/SPP1+ macrophages-monocytes, suggesting a spatial organized cellular crosstalk supporting fibrotic remodeling. Consistent with these findings, in vitro co-culture assays using ACKR1+ VECs isolated from IPF lungs demonstrate that these cells drive myeloid recruitment and fibroblast activation through ACKR1 dependent mechanisms. Silencing of ACKR1 in IPF-derived VECs suppressed inflammatory and fibrotic transcriptional programs, and pharmacological inhibition of ACKR1 attenuated stromal and immune remodeling and reduced bleomycin-induced lung fibrosis in vivo. Together, these findings identify ACKR1+ VECs as key orchestrators of fibrosis progression and establish ACKR1 and the pathogenic vasculature as promising therapeutic targets for IPF. - Source: PubMed
Publication date: 2026/08/03
Kontodimas KonstantinosRaslan Ahmed ASpira BenjaminChu UyenNarota ArunMurata HirokiHashimoto YasuakiNicosia Roberto FQiu XintaoHuang Steve KTrojanowska MariaVarelas XaralabosLigresti Giovanni - Nanobodies (Nbs) are new and promising tools for a variety of applications, including their use in medicine, although their functional activity and encounter with immune cells are still not well characterized. Our goal was to study the properties of Nbs coupled with the human IgG1 antibody Fc fragment (Nb-Fc), including their interaction with antigens, Fc receptors (FcRs), and professional phagocytes: macrophages. In our research, we employed a combination of two surface-sensitive methods: spectroscopic ellipsometry (SE) and quartz crystal microbalance with dissipation (QCM-D). It enabled the quantitative investigation of interaction kinetics between human FcγRI (CD64) and immune complexes (IC) formed by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein Wuhan variant (SCoV2-S) and specific Nb-Fc, as well as the optical and mechanical properties of the formed layers. Human THP-1 macrophage cell culture was used to analyze antigen and IC induced inflammatory response, antigen presentation-related processes, as well as chemokine CCL2/CCR2 and CCL5/CCR5 axes. Our investigated Nb-Fcs had a high affinity for SCoV2-S that was comparable to that of the natural human antibody CR3022. ICs formed by Nb-Fcs also interacted with FcRs in a similar way to CR3022. One of the investigated Nb-Fcs distinguished itself by its very high affinity and formed relatively the largest ICs. Interestingly, only ICs formed by the other Nb-Fcs influenced cellular response. We found increased cell surface expression of CD83. This molecule plays a regulatory role in antigen presentation and is involved in the resolution of inflammation following infection. In addition, we did not find any increase in other investigated markers in THP-1 macrophages, including the inflammatory response. Overall, our data demonstrate that Nb-Fcs can be applied in a similar manner to conventional human antibodies, considering their properties. - Source: PubMed
Publication date: 2026/08/19
Stančiauskaitė MiglėUsvaltas MantvydasMašalaitė KristinaLučiūnaitė AstaPlikusiene Ieva - Cryptococcal meningoencephalitis (CME) remains a leading cause of AIDS-related mortality, and up to one-quarter of persons living with HIV who survive CME develop cryptococcal immune reconstitution inflammatory syndrome (CME-IRIS) after antiretroviral therapy (ART) initiation. CME-IRIS arises when recovering immunity encounters a high residual fungal antigen burden, yet the temporal adaptive immune dynamics that distinguish protective reconstitution from damaging neuroinflammation are not fully defined. This review synthesizes clinical and experimental data to propose a temporal framework centered on CD4 T cell polarization, regulatory failure, memory T cell quality, and T-B cell coordination. Before ART, many patients exhibit a Th2-skewed, low-inflammatory state with impaired Th1 responses, reduced antifungal IgM production, and deficient Tfh-B cell coordination, collectively favoring persistent antigen burden. With ART, IL-7-driven T cell recovery, Th17/Treg imbalance, Th1/Th17-biased memory responses, and chemokine-guided trafficking of CXCR3CCR5 effector cells into the central nervous system can convert this antigen-rich milieu into fulminant neuroinflammation. We further discuss emerging mouse models that recapitulate unmasking CME-IRIS, the contrasting immune profile of -associated IRIS as a comparative model, and developing therapeutic strategies that include targeted immunomodulators, cell-based therapies, and vaccines. Finally, we highlight future directions - particularly single-cell and spatial transcriptomic profiling of blood and CSF - to resolve which adaptive immune populations drive neuroinflammation and to validate predictive biomarkers for CME-IRIS. A temporally informed view of adaptive immunity in CME-IRIS may refine ART timing, guide risk stratification, and identify new adjunctive interventions for cryptococcosis and related IRIS syndromes. - Source: PubMed
Publication date: 2026/07/24
Hunter MarcusMartinez Luis R