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
- 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 - To characterise early treatment-associated changes in circulating immune mediators following sirolimus initiation in patients with tocilizumab-resistant idiopathic multicentric Castleman disease (iMCD). - Source: PubMed
Publication date: 2026/08/14
Koga TomohiroFukui ShoichiSumiyoshi RemiShimizu ToshimasaHosogaya NaokiFukushima ChizuYamamoto HiroshiYoshifuji HajimeHiga ShinjiKawakami Atsushi - Diffuse midline gliomas (DMGs) are highly aggressive, WHO grade 4 glial tumors that arise in midline central nervous system structures and are defined by K27M mutations in histone H3 genes. These K27M mutations shape intratumoral myeloid cell composition in DMG. In H3.1K27M DMGs, genetic ablation of monocyte recruitment reshapes the tumor microenvironment (TME) by reducing monocyte-derived macrophages (MDMs) and increasing microglia and neutrophil presence, with overall survival remaining unchanged, indicating compensatory myeloid remodeling is occurring. Here, by using CRISPR/Cas9-based genome editing, we generated a mouse model deficient for CCR1/CCR2/CCR3/CCR5 (Δ1235). Using this strain, we effectively abolished monocyte and MDM infiltration and reversed compensatory recruitment of CCR1+ neutrophils. Abolishing MDMs in tumors skewed remaining neutrophils and microglia toward a homeostatic state, reduced expression of immune checkpoint molecules on T cells, and extended the survival of H3.1K27M DMG-bearing mice. In contrast, H3.3K27M DMG showed independence from MDM recruitment, suggesting reliance on other TME-driven signaling. Last, H3.1K27M DMGs exhibited reduced microglia presence and a dose-dependent increase in MDM infiltration postirradiation. MDM depletion did not further enhance radiation efficacy, potentially due to compensatory recruitment of classical neutrophils. Collectively, these data reveal histone mutation-specific myeloid dependencies in DMG, highlighting MDM-independent mechanisms in H3.3K27M tumors and MDM-dependent pathways in H3.1K27M tumors. - Source: PubMed
Publication date: 2026/08/13
Puigdelloses Vallcorba MontserratRawat KavitaSoni NishantDiMauro AngelaChu Jacqueline DThomason WesFurtado Glaucia CStrahl MayaWu JunyanJoshi TanviAngione AngeloPiñero GonzaloBecher Oren JRoss James LTsankov Alexander MLira Sergio AHambardzumyan Dolores - Invasion and metastasis in multiple solid tumors are promoted by collective invasion which is organized by leader and follower cells. Yet in colorectal cancer (CRC), biomarkers and mechanisms that specify leader cells remain undefined. Here we identify biomarkers of leader cells and elucidate how they drive CRC collective invasion and metastasis. Using a 3D photoconvertible CRC spheroid model, we isolated leader and follower cells. Transcriptomic, functional and in vivo assays show that GLUT1, PLOD2, and CCL5 in leader cells are indispensable for collective invasion. CCL5 activates PI3K/AKT signaling to up-regulate GLUT1 and PLOD2 in leader cells. Moreover, GLUT1 and CCL5 could serve as specific biomarkers for leader cells in CRC collective invasion, and their co-expression correlates with poor prognosis. Pharmacologic inhibition of GLUT1 and CCL5-CCR5 impairs collective invasion. CCL5 and GLUT1 may define the leader cells and are required for CRC collective invasion as potential key regulators of metabolic shifts and collagen deposition. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/08/12
Zhang ZhaowenTan JiayingZeng ZhichengZhu XiaohuiMai LiyaoYin YaoHuang YutingKang WeiJiang HonghuiXu ShaowanDing YanqingPan XinghuaWang FeifeiLiang Li - Few studies have evaluated the impact of organ-specific tumor microenvironments (TMEs) on clinical outcomes in diffuse large B-cell lymphoma (DLBCL). This study investigated potential molecular markers, the immune cell composition within the TME, and their associations with clinical outcomes in patients with primary intestinal DLBCL (PI-DLBCL). We initially analyzed RNA expression in tumor cells from 19 patients with PI-DLBCL in the experimental cohort. Candidate biomarkers were then assessed in lymphoma tissue from a total of 48 patients in the same cohort, including the 19 with RNA-expression data, and validated in an independent cohort of 29 patients with PI-DLBCL. Associations between these markers and clinicopathological features, event-free survival (EFS), and overall survival (OS) in the two cohorts were analyzed. In the RNA expression panel, CCL5 expression was higher in patients with advanced-stage PI-DLBCL and was associated with inferior EFS and OS. Its principal receptor, CCR5, expressed in approximately one-third of patients, was associated with lower complete response rates to first-line immunochemotherapy: 50% in the experimental cohort and 10% in the validation cohort and correlated with the 7-year worse OS rate in both the experimental (49.8% versus 71.4%, p = 0.082) and validation (0% versus 76.2%, p < 0.001) cohorts. In both the experimental and validation cohorts, CCR5-positive tumors exhibited decreased CD86-positive (M1-like) and increased CD206-positive (M2-like) macrophage infiltration, consistent with an immunosuppressive TME. Multivariate analyses revealed that CCR5 expression was independently associated with worse EFS (p < 0.001) and OS (p = 0.004) in patients with PI-DLBCL (combined experimental and validation cohorts). CCR5 expression indicates a biologically aggressive subtype of PI-DLBCL with poor clinical outcomes and M2 macrophage-dominant immunosuppression. - Source: PubMed
Ma Wei-LiChen Tsai-YunFu Pei-AnChen Jo-PaiYao MingWang Hsiu-PoLin Been-RenLin Chung-WuHsu Chia-LangHuang Chung-YuCheng Ann-LiiKuo Sung-Hsin