Last update 01 Nov 2024

CCR1 x CCR3

Last update 01 Nov 2024

Basic Info

Related Targets

CCR1CCR3

Drugs associated with CCR1 x CCR3

SSFF-02

Target

CCR1 x CCR3 x CCR5

Mechanism

CCR1 antagonists [+2]

Active Org.

University of Texas at El Paso

Originator Org.

University of Texas at El Paso

Active Indication

Breast Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

J-113863

Target

CCR1 x CCR3

Mechanism

CCR1 antagonists [+1]

Active Org.-

Originator Org.

Banyu Pharmaceutical Co. Ltd.

Active Indication-

Inactive Indication

Multiple Sclerosis [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CCR1 x CCR3

100 Translational Medicine associated with CCR1 x CCR3

0 Patents (Medical) associated with CCR1 x CCR3

344

Literatures (Medical) associated with CCR1 x CCR3

15 Jul 2024·The Journal of Immunology

CCR1 and CCR2 Coexpression on Monocytes Is Nonredundant and Delineates a Distinct Monocyte Subpopulation

Article

Author: Mathie, Heather ; Medina-Ruiz, Laura ; Graham, Gerard J. ; Halawa, Heba A. ; Bartolini, Robin ; Schuette, Fabian ; Cunningham, Madeleine

AbstractThe interactions between chemokines and their receptors, particularly in the context of inflammation, are complex, with individual receptors binding multiple ligands and individual ligands interacting with multiple receptors. In addition, there are numerous reports of simultaneous coexpression of multiple inflammatory chemokine receptors on individual inflammatory leukocyte subtypes. Overall, this has previously been interpreted as redundancy and proposed as a protective mechanism to ensure that the inflammatory response is robust. By contrast, we have hypothesized that the system is not redundant but exquisitely subtle. Our interests relate to the receptors CCR1, CCR2, CCR3, and CCR5, which, together, regulate nonneutrophilic myeloid cell recruitment to inflammatory sites. In this study, we demonstrate that although most murine monocytes exclusively express CCR2, there is a small subpopulation that is expanded during inflammation and coexpresses CCR1 and CCR2. Combinations of transcript and functional analysis demonstrate that this is not redundant expression and that coexpression of CCR1 and CCR2 marks a phenotypically distinct population of monocytes characterized by expression of genes otherwise typically associated with neutrophils. Single-cell RNA sequencing confirms this as a monodisperse population of atypical monocytes. This monocytic population has previously been described as having immunosuppressive activity. Overall, our data confirm combinatorial chemokine receptor expression by a subpopulation of monocytes but demonstrate that this is not redundant expression and marks a discrete monocytic population.

01 Jul 2024·Journal of Psychiatric Research

Greater methylation of the IL-6 promoter region is associated with decreased integrity of the corpus callosum in schizophrenia

Article

Author: Bielecki, Maksymilian ; Plichta, Piotr ; Andrusewicz, Wojciech ; Misiak, Błażej ; Tyburski, Ernest ; Samochowiec, Jerzy ; Cecerska-Heryć, Elżbieta ; Rudkowski, Krzysztof ; Michalczyk, Anna ; Mak, Monika ; Rek-Owodziń, Katarzyna ; Waszczuk, Katarzyna ; Sagan, Leszek ; Podwalski, Piotr ; Kucharska-Mazur, Jolanta ; Samochowiec, Agnieszka

BACKGROUNDSchizophrenia is associated with chronic subclinical inflammation and decreased integrity of the corpus callosum (CC). Our previous study showed associations between peripheral IL-6 levels and the integrity of the CC. Epigenetic studies show associations between methylation of the genes related to immunological processes and integrity of the CC.AIMTo investigate correlations between methylation status of IL-6 promotor and peripheral IL-6 levels and the integrity of the CC in schizophrenia.MATERIAL AND METHODSThe participants were 29 chronic schizophrenia patients (SCH) and 29 controls. Decreased integrity of the CC was understood as increased mean diffusivity (MD) and/or decreased fractional anisotropy (FA) in diffusion tensor imaging. Peripheral IL-6 concentrations were measured in serum samples and IL-6 promoter methylation status of 6 CpG sites was analyzed in peripheral leukocytes by pyrosequencing.RESULTSModerate positive correlations were found between CpG1 methylation and the MD of proximal regions of the CC (CCR1-CCR3) and between CpG_mean and MD of CCR1 in SCH. Weaker positive correlations were found for CpG_mean with CCR2 and CCR3 and negative correlations were found for CpG1 and FA of CCR3 in SCH. Multivariate regression showed that methylation of CpG1, type of antipsychotic treatment, and their interaction were significant independent predictors of MD of CCR1 in SCH. Methylation of CpG2 was negatively correlated with serum IL-6 in SCH.CONCLUSIONSThe methylation level of the IL-6 promotor region in peripheral leukocytes is associated with the integrity of the CC in schizophrenia and this association may depend on the type of antipsychotic treatment. Further studies are necessary to explain the mechanisms of the observed associations.

14 Jun 2024·Science Advances

MAIT cell activation and recruitment in inflammation and tissue damage in acute appendicitis

Article

Author: Leeansyah, Edwin ; Lobie, Peter E ; Boulouis, Caroline ; Han, Fei ; Ho, Amanda ; Sia, Wan Rong ; Sandberg, Johan K ; Chen, Xingchi ; Zheng, Yichao ; He, Dan ; Jiang, Yuebin ; Wu, Zhengyu ; Wang, Lin-Fa ; Ma, Shaohua ; Mak, Jeffrey Y W ; Fairlie, David P ; Wang, Bingjie

Mucosal-associated invariant T (MAIT) cells are antimicrobial T cells abundant in the gut, but mechanisms for their migration into tissues during inflammation are poorly understood. Here, we used acute pediatric appendicitis (APA), a model of acute intestinal inflammation, to examine these migration mechanisms. MAIT cells were lower in numbers in circulation of patients with APA but were enriched in the inflamed appendix with increased production of proinflammatory cytokines. Using the patient-derived appendix organoid (PDAO) model, we found that circulating MAIT cells treated with inflammatory cytokines elevated in APA up-regulated chemokine receptors, including CCR1, CCR3, and CCR4. They exhibited enhanced infiltration of Escherichia coli –pulsed PDAO in a CCR1-, CCR2-, and CCR4-dependent manner. Close interactions of MAIT cells with infected organoids led to the PDAO structural destruction and death. These findings reveal a previously unidentified mechanism of MAIT cell tissue homing, their participation in tissue damage in APA, and their intricate relationship with mucosal tissues during acute intestinal inflammation in humans.

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