ELISA Mouse , IP-10
- Known as:
- Enzyme-linked immunosorbent assay test Mouse , IP-10
- Catalog number:
- RBMS6018R
- Product Quantity:
- 96 wells (1 kit)
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- ELISA Mouse IP-10
Related genes to: ELISA Mouse , IP-10
- Gene:
- BBIP1 NIH gene
- Name:
- BBSome interacting protein 1
- Previous symbol:
- NCRNA00081
- Synonyms:
- bA348N5.3, BBIP10, BBS18
- Chromosome:
- 10q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2008-09-02
- Date modifiied:
- 2016-10-05
- Gene:
- CXCR3 NIH gene
- Name:
- C-X-C motif chemokine receptor 3
- Previous symbol:
- GPR9
- Synonyms:
- CKR-L2, CMKAR3, IP10-R, MigR, CD183
- Chromosome:
- Xq13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-01
- Date modifiied:
- 2016-10-05
- Gene:
- MED24 NIH gene
- Name:
- mediator complex subunit 24
- Previous symbol:
- THRAP4, CRSP4
- Synonyms:
- TRAP100, KIAA0130, DRIP100, CRSP100, MED5
- Chromosome:
- 17q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-30
- Date modifiied:
- 2016-10-05
- Gene:
- PPIAP10 NIH gene
- Name:
- peptidylprolyl isomerase A pseudogene 10
- Previous symbol:
- PPIAL2, PPIP10
- Synonyms:
- CRP
- Chromosome:
- 20q13.2
- Locus Type:
- pseudogene
- Date approved:
- 1998-10-12
- Date modifiied:
- 2017-08-21
- Gene:
- PRPF40A NIH gene
- Name:
- pre-mRNA processing factor 40 homolog A
- Previous symbol:
- FNBP3
- Synonyms:
- FLJ20585, FBP11, HYPA, NY-REN-6, HIP10, FBP-11, FLAF1, Prp40
- Chromosome:
- 2q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-28
- Date modifiied:
- 2018-11-19
Related products to: ELISA Mouse , IP-10
Related articles to: ELISA Mouse , IP-10
- SARS-CoV-2-associated hepatobiliary injury and biliary atresia (BA) differ markedly in etiology and biological context, but both involve injury to the biliary epithelial compartment. Here, we performed integrative transcriptomic and single-cell analyses to investigate whether these distinct hepatobiliary injury contexts converge on a shared cholangiocyte-associated inflammatory host-response program. Bulk transcriptomic datasets from SARS-CoV-2-infected human liver organoids and BA liver tissues were integrated to identify shared transcriptional alterations, followed by functional enrichment, protein-protein interaction, regulatory network, drug-gene interaction, and molecular docking analyses. Single-nucleus and single-cell datasets were used to determine the cellular localization of the shared program, and key findings were further assessed in BA liver tissues and cultured human cholangiocytes exposed to poly(I:C). We identified an expanded exploratory set of 164 shared genes and a stringent -adjusted core of 52 genes. Both sets consistently implicated antiviral defense, type I and type II interferon signaling, double-stranded RNA responses, and cytokine and chemokine signaling. STAT1, ISG15, and CXCL10 were retained in the stringent core and remained central components of the interaction network. In COVID-19 liver single-nucleus data, donor-level analysis showed preferential localization of the shared signature to cholangiocytes, whose mean scores were significantly higher than those of all other hepatic cells combined ( = 0.00368). A similar pattern was observed descriptively in our BA single-nucleus dataset and further supported by an independent BA single-cell cohort. Tissue immunofluorescence spatially associated pSTAT1, total STAT1, and ISG15 signals with KRT19-positive ductular structures, whereas CXCL10 was predominantly periductal. Poly(I:C) stimulation induced representative components of the program in cultured cholangiocytes. Computational analyses retained mefloquine among the top-ranked exploratory candidates. Collectively, these findings support a convergent cholangiocyte-associated interferon/inflammatory host-response program in BA and SARS-CoV-2-associated hepatobiliary injury. They indicate molecular association rather than a common etiology or causal relationship and provide testable hypotheses for further investigation of biliary epithelial inflammatory responses. - Source: PubMed
Publication date: 2026/09/16
Wa YujuanGuan RongDu ZhanweiLin RouchenCui ShiyuGuang JiangleiXu LidanJi WeiYang QianCui QingboWang HaoSun Wenjing - Marmosets (MAR, Callithrix jacchus) are nonhuman primates extensively studied in a broad array of preclinical biomedical research areas. However, the limited number of available immunological reagents remains a critical shortcoming of these models. We successfully developed monoclonal antibodies (mAbs) pairs that can be used in immunoassays for the identification and quantification of the biomarkers of inflammation C-reactive protein (CRP), CXCL-10 (IP-10), interleukin (IL)-4, IL-6, and IL-10. Recombinant MAR protein variants were produced in mammalian cells, purified and used for mice immunization. Hybridoma clones were selected first for their capacity to bind the recombinant proteins. All possible pair combinations of these mAbs were then tested for their capacity to identify their targets in MAR-derived samples. These MAR samples consisted of supernatant of PBMCs exposed ex vivo to different stimulants, and plasma samples from animals stimulated in vivo with a low-dose intravenous LPS inoculation. The majority of the mAbs that recognized the recombinant proteins failed to bind to the MAR-derived homologs. However, we found MAR-derived reactive mAbs and selected pairs with optimal sensitivity and signal-to-noise ratio for immunoassays that included Luminex multiplexing assays, ELISA, and ELISpot assays. These immunoreagents and assays will improve the translational value of different MAR biomedical models. - Source: PubMed
Publication date: 2026/09/23
Lambrou EktorasHallengärd DavidTurbow BenjaminCallery JessicaHodara VidaKing JonathanRoss CorinnaAhlborg NiklasMakower BartekGiavedoni Luis D - Extracellular vesicles (EVs) moderate a variety of physiological and pathological processes by enabling the intercellular transfer of proteins, nucleic acids, and lipids. Bioactive lipids such as polyunsaturated fatty acids or eicosanoids play an important role in propagation and resolution of inflammation and in vascular regulation. We previously found that the lipid composition of macrophage-derived EVs depends on polarization of the originating macrophages. - Source: PubMed
Publication date: 2026/10/01
Shamkeeva SaikalAmbreen SairaJiang ShihaiReinicke MadlenLi ZhiyangRana RajivElwakiel AhmedSchmidt CarolineWagner UlfIsermann BerendCeglarek UtaHeinemann Mitja L - Vitiligo-like depigmentation (VLD) arising under immune checkpoint blockade in melanoma is associated with objective tumour response and substantially longer survival. Its prognostic value is not coincidental: depigmentation and tumour regression share a CD8⁺ effector programme directed at melanocyte differentiation antigens and recruited through the IFN-γ-CXCL9/CXCL10-CXCR3 axis, an axis independently required for the efficacy of PD-1 blockade. The depigmenting lesion is therefore an accessible compartment in which the antitumour effector response could, in principle, be measured directly. This opportunity is currently unexploited: VLD is graded by inspection, and its molecular correlates are sought almost exclusively in plasma, where a locally generated chemokine signal is diluted into a whole-body average confounded by tumour burden, concurrent immune-related adverse events and corticosteroid exposure. Paired-matrix data from spontaneous vitiligo show that the same chemokines discriminate active from stable depigmentation several-fold in lesional skin interstitial fluid whilst discriminating poorly in serum from the same patients, a finding not yet tested in the ICI setting. Building on this observation as an explicit hypothesis, we reframe the problem as one of matrix selection, pre-analytical control and analytical validation: we compare skin-proximal and systemic matrices against tumour biopsy and circulating tumour DNA, define the pre-analytical variables that are peculiar to oncology, and outline a translational roadmap by which a validated cutaneous assay could convert a visible prognostic sign into a quantitative, early and repeatable readout of antitumour immunity. - Source: PubMed
Publication date: 2026/09/30
Toshev SuhrobJalalova DilfuzaTastanova GulchekhraNurmatova IrodaLatipov IkhtiyorIsmoilov Ortiq - Herpes simplex virus type 2 (HSV-2) infects genital epithelia and causes a wide spectrum of clinical outcomes, ranging from asymptomatic viral shedding to recurrent self-limited genital lesions. Interferon gamma (IFNγ) is critical in tissue-resident T-cell mediated antiviral defense against HSV-2 reactivation. However, the responsiveness of epithelial cells to IFNγ and its contribution to disease variability remains poorly understood. Here we investigated IFNγ-mediated antiviral responses in primary keratinocytes and donor-matched fibroblasts from individuals with either asymptomatic or ulcerative HSV-2 infection. Our results revealed that keratinocytes are remarkably sensitive to IFNγ, with altered gene expression observed at doses much lower than previously reported. Keratinocytes exhibited greater sensitivity to IFNγ stimulation than fibroblasts, including robust induction of chemokines involved in immune cell recruitment. Among them, CXCL10 was the most sensitive and strongly induced gene, displaying rapid upregulation even at low IFNγ concentrations. Notably, keratinocytes from individuals with asymptomatic HSV-2 infection exhibited significantly greater IFNγ responses at both the mRNA and protein levels compared with those from symptomatic donors, particularly at physiologically low IFNγ doses. This heightened responsiveness was associated with increased nuclear localization of phosphorylated STAT1 following IFNγ stimulation, despite similar baseline expression of IFNγ receptor and STAT1 across donor groups. While IFNγ pretreatment similarly inhibited HSV replication in keratinocytes from both cohorts, the enhanced chemokine production by keratinocytes from asymptomatic individuals may promote more efficient recruitment of antiviral immune cells. Together, these findings identify intrinsic variation in epithelial IFNγ signaling as a potential host factor associated with clinical outcomes in HSV infection. The results suggest that CXCL10-mediated immune recruitment might be a key mechanism linking tissue-resident T cell cytokine signaling to epithelial antiviral defense. Understanding variability in epithelial barrier immune defense may be crucial to improving therapies and vaccine strategies for genital herpes infection. - Source: PubMed
Publication date: 2026/09/30
Zimenko AngelinaHayman IanFong YouyiMonroe Luke DMills Margaret GGreninger AlexJohnston ChristineCorey LawrenceZhu Jia