CLIA CMK,C-X-C motif chemokine 9,CXCL9,Gamma-interferon-induced monokine,Homo sapiens,Human,HuMIG,MIG,MIG,Monokine induced by interferon-gamma,SCYB9,Small-inducible cytokine B9
- Known as:
- CLIA CMK,C-X-C motif chemokine 9,CXCL9,Gamma-IFN-induced monokine,Homo sapiens,Human,HuMIG,MIG,MIG,Monokine induced IFN-g,SCYB9,Small-inducible cytokine B9
- Catalog number:
- U1928h
- Product Quantity:
- 96T
- Category:
- -
- Supplier:
- EIAab
- Gene target:
- CLIA CMK C-X- motif chemokine 9 CXCL9 Gamma-interferon-induced monokine Homo sapiens Human HuMIG MIG Monokine induced interferon-gamma SCYB9 Small-inducible cytokine B9
Related genes to: CLIA CMK,C-X-C motif chemokine 9,CXCL9,Gamma-interferon-induced monokine,Homo sapiens,Human,HuMIG,MIG,MIG,Monokine induced by interferon-gamma,SCYB9,Small-inducible cytokine B9
- Gene:
- ABCA7 NIH gene
- Name:
- ATP binding cassette subfamily A member 7
- Previous symbol:
- -
- Synonyms:
- ABCX
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-11
- Date modifiied:
- 2019-03-21
- Gene:
- ACKR3 NIH gene
- Name:
- atypical chemokine receptor 3
- Previous symbol:
- CMKOR1, CXCR7
- Synonyms:
- RDC1, GPR159
- Chromosome:
- 2q37.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-01
- Date modifiied:
- 2014-11-19
- Gene:
- ACKR4 NIH gene
- Name:
- atypical chemokine receptor 4
- Previous symbol:
- CCRL1
- Synonyms:
- CCR11, CCBP2, VSHK1, CCX-CKR, PPR1
- Chromosome:
- 3q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-18
- Date modifiied:
- 2016-10-05
- Gene:
- AKAP17A NIH gene
- Name:
- A-kinase anchoring protein 17A
- Previous symbol:
- CXYorf3, SFRS17A
- Synonyms:
- XE7, XE7Y, DXYS155E, MGC39904, 721P, CCDC133
- Chromosome:
- Xp22.33 and Yp11.32
- Locus Type:
- gene with protein product
- Date approved:
- 2006-09-22
- Date modifiied:
- 2015-11-17
- Gene:
- ALG13 NIH gene
- Name:
- ALG13 UDP-N-acetylglucosaminyltransferase subunit
- Previous symbol:
- GLT28D1, CXorf45
- Synonyms:
- MDS031, YGL047W, FLJ23018, TDRD13, CDG1S
- Chromosome:
- Xq23
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-16
- Date modifiied:
- 2019-01-18
Related products to: CLIA CMK,C-X-C motif chemokine 9,CXCL9,Gamma-interferon-induced monokine,Homo sapiens,Human,HuMIG,MIG,MIG,Monokine induced by interferon-gamma,SCYB9,Small-inducible cytokine B9
Related articles to: CLIA CMK,C-X-C motif chemokine 9,CXCL9,Gamma-interferon-induced monokine,Homo sapiens,Human,HuMIG,MIG,MIG,Monokine induced by interferon-gamma,SCYB9,Small-inducible cytokine B9
- Tick-borne encephalitis virus (TBEV) and West Nile virus (WNV) are the most important neuroinvasive arboviruses detected in Europe. In this study, we analyzed cerebrospinal fluid (CSF) concentrations of 12 proinflammatory chemokines (CCL2, CCL3, CCL4, CCL11, CCL17, CCL20, CXCL1, CXCL5, CXCL8, CXCL9, CXCL10, and CXCL11) in 77 patients with neuroinvasive diseases (NIDs). Flavivirus infection was confirmed in 62 patients (TBEV and WNV in 31 patients each), while in 15 patients the etiology of NID was not determined (NDE). Similar patterns of high-level expression of chemokines regulating monocyte/macrophage responses (CCL2), neutrophil recruitment (CXCL1 and CXCL8), and interferon-inducible chemoattractants for leukocytes (CXCL10 and CXCL11) have been observed in WNV and TBEV groups. None of the tested chemokines significantly differed between patients with TBEV or WNV. Concentrations of CCL17, CCL20, CXCL5, CXCL10, and CXCL11 were significantly lower in both WNV and TBEV groups compared to NID NDE patients. The logistic regression model showed that CSF concentrations of CXCL11, CXCL5, and CXCL10 could potentially be used for the classification of patients into the WNV or TBEV group versus groups with other NIDs. This study identified, for the first time, similar patterns of CSF chemokine expression in WNV and TBEV infections, suggesting common immunopathogenic mechanisms in neuroinvasive flavivirus infections that should be further evaluated. - Source: PubMed
Publication date: 2024/03/26
Zidovec-Lepej SnjezanaBodulić KristianBogdanic MajaGorenec LanaSavic VladimirGrgic IvanaSabadi DarioSantini MarijaRadmanic Matotek LeonaKucinar JasminaBarbic LjuboZmak LjiljanaFerenc ThomasStevanovic VladimirAntolasic LjiljanaMilasincic LjiljanaHruskar ZeljkaVujica Ferenc MatejaVilibic-Cavlek Tatjana - Pleural biomarkers represent potential diagnostic tools for tuberculous pleural effusion (TPE) due to their advantages of low cost, short turnaround time, and less invasiveness. This study evaluated the diagnostic accuracy of two CXCR3 ligands, C-X-C motif chemokine ligand 9 (CXCL9) and CXCL11, for TPE. In addition, we investigated the cellular origins and biological roles of CXCL9 and CXCL11 in the development of TPE. - Source: PubMed
Publication date: 2024/04/24
Yan ZhiWen Jian-XunNiu YanJiang Ting-WangHuang Jin-HongChen HongChen QiWang Ya-FeiYan LiHu Zhi-DeZheng Wen-Qi - Alopecia areata (AA) is an autoimmune disease characterized by damage to hair follicles and hair loss. Cell-free DNA (cfDNA) has recently received attention as a biomarker of various disorders including inflammatory skin diseases. In this study, we aimed to investigate the clinical significance of cfDNA and the circulating DNAs of disease-associated cytokines in AA patients. Serum samples were obtained from 63 patients with AA and 32 healthy controls (HC). Using droplet digital polymerase chain reaction, circulating C-X-C motif chemokine ligand (CXCL) 9, CXCL10, CXCL11, C-X-C motif chemokine receptor 3, interferon (IFN)-γ, interleukin (IL) -7, IL-15, and Janus kinase (JAK) 2 were detectable in both HC and AA patients. Among the detectable DNAs, copies of circulating CXCL9, CXCL11, IL-15, IFN-γ, and JAK2 were significantly higher in AA patients than in HC. These results suggest that increased circulating DNA levels may reflect damage to hair follicles in AA patients. - Source: PubMed
Publication date: 2024/04/13
Sawamura SoichiroMyangat Tselmeg MKajihara IkkoMakino KatsunariAoi JunMasuguchi ShinichiFukushima Satoshi - In atherosclerotic lesions, monocyte-derived macrophages are major source of interferon gamma (IFN-γ), a pleotropic cytokine known to regulate the expression of numerous genes, including the antiviral gene RSAD2. While RSAD2 was reported to be expressed in endothelial cells of human carotid lesions, its significance for the development of atherosclerosis remains utterly unknown. Here, we harnessed publicly available human carotid atherosclerotic data to explore RSAD2 in lesions and employed siRNA-mediated gene-knockdown to investigate its function in IFN-γ-stimulated human aortic smooth muscle cells (hAoSMCs). Silencing RSAD2 in IFN-γ-stimulated hAoSMCs resulted in reduced expression and secretion of key CXCR3-chemokines, CXCL9, CXCL10, and CXCL11. Conditioned medium from RSAD2-deficient hAoSMCs exhibited diminished monocyte attraction in vitro compared to conditioned medium from control cells. Furthermore, RSAD2 transcript was elevated in carotid lesions where it was expressed by several different cell types, including endothelial cells, macrophages and smooth muscle cells. Interestingly, RSAD2 displayed significant correlations with CXCL10 (r = 0.45, p = 0.010) and CXCL11 (r = 0.53, p = 0.002) in human carotid lesions. Combining our findings, we uncover a novel role for RSAD2 in hAoSMCs, which could potentially contribute to monocyte recruitment in the context of atherosclerosis. - Source: PubMed
Publication date: 2024/04/08
Hayderi AssimKumawat Ashok KShavva Vladimir SDreifaldt MatsSigvant BirgittaPetri Marcelo HKragsterman BjörnOlofsson Peder SSirsjö AllanLjungberg Liza U - Following acute herpes simplex virus type 2 (HSV-2) infection, the virus undergoes an asymptomatic latent infection of sensory neurons of dorsal root ganglia (DRG). Chemical and physical stress cause intermittent virus reactivation from latently infected DRG and recurrent virus shedding in the genital mucosal epithelium causing genital herpes in symptomatic patients. While T cells appear to play a role in controlling virus reactivation from DRG and reducing the severity of recurrent genital herpes, the mechanisms for recruiting these T cells into DRG and the vaginal mucosa (VM) remain to be fully elucidated. The present study investigates the effect of CXCL9, CXCL10, and CXCL11 T-cell-attracting chemokines on the frequency and function of DRG- and VM-resident CD4 and CD8 T cells and its effect on the frequency and severity of recurrent genital herpes in the recurrent herpes guinea pig model. HSV-2 latent-infected guinea pigs were immunized intramuscularly with the HSV-2 ribonucleotide reductase 2 (RR2) protein () and subsequently treated intravaginally with the neurotropic adeno-associated virus type 8 expressing CXCL9, CXCL10, or CXCL11 chemokines to recruit CD4 and CD8 T cells into the infected DRG and VM (). Compared to the RR2 therapeutic vaccine alone, the RR2/CXCL11 prime/pull therapeutic vaccine significantly increased the frequencies of functional tissue-resident and effector memory CD4 and CD8 T cells in both DRG and VM tissues. This was associated with less virus in the healed genital mucosal epithelium and reduced frequency and severity of recurrent genital herpes. These findings confirm the role of local DRG- and VM-resident CD4 and CD8 T cells in reducing virus shedding at the vaginal site of infection and the severity of recurrent genital herpes and propose the novel prime-pull vaccine strategy to protect against recurrent genital herpes.IMPORTANCEThe present study investigates the novel prime/pull therapeutic vaccine strategy to protect against recurrent genital herpes using the latently infected guinea pig model. In this study, we used the strategy that involves immunization of herpes simplex virus type 2-infected guinea pigs using a recombinantly expressed herpes tegument protein-ribonucleotide reductase 2 (RR2; prime), followed by intravaginal treatment with the neurotropic adeno-associated virus type 8 expressing CXCL9, CXCL10, or CXCL11 T-cell-attracting chemokines to recruit T cells into the infected dorsal root ganglia (DRG) and vaginal mucosa (VM) (pull). We show that the RR2/CXCL11 prime-pull therapeutic vaccine strategy elicited a significant reduction in virus shedding in the vaginal mucosa and decreased the severity and frequency of recurrent genital herpes. This protection was associated with increased frequencies of functional tissue-resident (T cells) and effector (T cells) memory CD4 and CD8 T cells infiltrating latently infected DRG tissues and the healed regions of the vaginal mucosa. These findings shed light on the role of tissue-resident and effector memory CD4 and CD8 T cells in DRG tissues and the VM in protection against recurrent genital herpes and propose the prime-pull therapeutic vaccine strategy in combating genital herpes. - Source: PubMed
Publication date: 2024/04/08
Quadiri AfshanaPrakash SwayamDhanushkodi Nisha RajeswariSinger MahmoudZayou LatifaShaik Amin MohammedSun MiyoSuzer BerfinLau Lauren Su LinChilukurri AmruthVahed HawaSchaefer HubertBenMohamed Lbachir