更新于：2024-11-01

CXCL9 x CXCL11 x CCL5 x CCL20 x CCL2 x Chemokine receptors x CXCL10

更新于：2024-11-01

基本信息

关联

项与 CXCL9 x CXCL11 x CCL5 x CCL20 x CCL2 x Chemokine receptors x CXCL10 相关的药物

BKT-130

靶点

CCL2 x CCL20 x CCL5 x CXCL10 x CXCL11 x CXCL9

作用机制

CCL2抑制剂 [+6]

在研机构

Biokine Therapeutics Ltd. [+1]

原研机构

Biokine Therapeutics Ltd.

在研适应症

脉络膜新生血管 [+3]

非在研适应症

肿瘤

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 CXCL9 x CXCL11 x CCL5 x CCL20 x CCL2 x Chemokine receptors x CXCL10 相关的临床结果

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100 项与 CXCL9 x CXCL11 x CCL5 x CCL20 x CCL2 x Chemokine receptors x CXCL10 相关的转化医学

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0 项与 CXCL9 x CXCL11 x CCL5 x CCL20 x CCL2 x Chemokine receptors x CXCL10 相关的专利（医药）

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项与 CXCL9 x CXCL11 x CCL5 x CCL20 x CCL2 x Chemokine receptors x CXCL10 相关的文献（医药）

2016-01-01·Mediators of Inflammation3区 · 医学

Doxycycline and Benznidazole Reduce the Profile of Th1, Th2, and Th17 Chemokines and Chemokine Receptors in Cardiac Tissue from ChronicTrypanosoma cruzi-Infected Dogs

3区 · 医学

ArticleOA

作者: Milanezi, Cristiane M. ; Lopes, Laís Roquete ; Guedes, Paulo Marcos da Mata ; Schulz, Richard ; Silva, Maria Cláudia da ; Paula Costa, Guilherme de ; Silva, João Santana da ; Pontes, Washington Martins ; Lima, Wanderson Geraldo de ; Horta, Aline Luciano ; Talvani, Andre

Chemokines (CKs) and chemokine receptors (CKR) promote leukocyte recruitment into cardiac tissue infected by theTrypanosoma cruzi. This study investigated the long-term treatment with subantimicrobial doses of doxycycline (Dox) in association, or not, with benznidazole (Bz) on the expression of CK and CKR in cardiac tissue. Thirty mongrel dogs were infected, or not, with the Berenice-78 strain ofT. cruziand grouped according their treatments: (i) two months after infection, Dox (50 mg/kg) 2x/day for 12 months; (ii) nine months after infection, Bz (3,5 mg/kg) 2x/day for 60 days; (iii) Dox + Bz; and (iv) vehicle. After 14 months of infection, hearts were excised and processed for qPCR analysis of Th1 (CCL2, CCL3, CCL4, CCL5, CXCL9, and CXCL11), Th2 (CCL1, CCL17, CCL24, and CCL26), Th17 (CCL20) CKs, Th1 (CCR5, CCR6, and CXCR3), and Th2/Th17 (CCR3, CCR4, and CCR8) CKR, as well as IL-17.T. cruziinfection increases CCL1, CCL2, CCL4, CCL5, CCL17, CXCL10, and CCR5 expression in the heart. Dox, Bz, or Dox + Bz treatments cause a reversal of CK and CKR and reduce the expression of CCL20, IL-17, CCR6, and CXCR3. Our data reveal an immune modulatory effect of Dox with Bz, during the chronic phase of infection suggesting a promising therapy for cardiac protection.

2011-03-01·Radiation and Environmental Biophysics4区 · 环境科学与生态学

Analysis of chemokine and chemokine receptor expression in squamous cell carcinoma of the head and neck (SCCHN) cell lines

4区 · 环境科学与生态学

Article

作者: Hans Christiansen ; Wolfgang Eicheler ; Ralph M. W. Rödel ; Markus Schirmer ; Andrea Hille ; Hendrik A. Wolff ; Annegret Doerfler ; David Rolke ; Clemens F. Hess ; Christoph Matthias ; Margret Rave-Fränk

The purpose of this work was to analyze chemokine and chemokine receptor expression in untreated and in irradiated squamous cell carcinoma of the head and neck (SCCHN) tumor cell lines, aiming at the establishment of assays to test for the relevance of chemokine and chemokine receptor expression in the response of SCCHN to radiotherapy and radiochemotherapy. Five low passage and 10 established SCCHN lines, as well as two normal cell lines, were irradiated at 2 Gy or sham-irradiated, and harvested between 1 and 48 h after treatment. For chemokines with CC and CXC structural motifs and their receptors, transcript levels of target and reference genes were quantified relatively by real-time PCR. In addition, CXCL1 and CXCL12 protein expression was analyzed by ELISA. A substantial variation in chemokine and chemokine receptor expression between SCCHN was detected. Practically, all cell lines expressed CCL5 and CCL20, while CCL2 was expressed in normal cells and in some of the tumor cell lines. CXCL1, CXCL2, CXCL3, CXCL10, and CXCL11 were expressed in the vast majority of the cell lines, while the expression of CXCL9 and CXCL12 was restricted to fibroblasts and few tumor cell lines. None of the analyzed cell lines expressed the chemokines CCL3, CCL4, or CCL19. Of the receptors, transcript expression of CCR1, CCR2, CCR3, CCR5, CCR7, CCXR2, and CCXR3 was not detected, and CCR6, CXCR1, and CXCR4 expression was restricted to few tumor cells. Radiation caused up- and down-regulation with respect to chemokine expressions, while for chemokine receptor expressions down-regulations were prevailing. CXCL1 and CXCL12 protein expression corresponded well with the mRNA expression. We conclude that the substantial variation in chemokine and chemokine receptor expression between SCCHN offer opportunities for the establishment of assays to test for the relevance of chemokine and chemokine receptor expression in the response of SCCHN to radiotherapy and radiochemotherapy.