CloneID: CXCR3-173
Antigen Long Description: The original antibody was generated by immunizing Armenian hamsters with a multiple antigen peptide (MAPS8) encompassing amino acids 1-37 of mouse CXCR3 in complete Freund's adjuvant, and boosted with peptide in incomplete Freund's adjuvant.
Buffer Composition: PBS with 0.02% Proclin 300.
Available Custom Conjugation Options: AP, HRP, Fluorescein, APC, PE, Biotin Type A, Biotin Type B, Streptavidin, FluoroProbes 647H, Atto488, APC/Cy7, PE/Cy7
Uniprot Accession No.: O88410
Specificity Statement: This antibody is specific for mouse CXCR3 and recognizes CXCR3 on cells from wild-type but not CXCR3-/- mice.
Application Notes (Clone): This antibody’s original format (hamster (Armenian) IgG) was used in ligand binding assay (LBA), FACS-based chemokine binding inhibition assay, and chemotaxis assays, as well as to measure its pharmacokinetics and immunogenicity in a mouse model. It blocked chemotaxis in response to CXCL10 or CXCL11 in vitro. When injected into mice, this antibody significantly prolonged cardiac and islet allograft survival. When combined with a subtherapeutic regimen of rapamycin, this antibody induced long-term (>100 d) survival of cardiac and islet allografts (Uppaluri et al., 2008; PMID: 18622291). This antibody was used to block CXCR3 to investigate its role in lymphocyte migration in vivo. The antibody was given intravenously just before an injection of labeled T cells to assess the effect of blocking CXCR3 on T cell migration (Dai et al., 2016; PMID: 27412416). This antibody was used as an anti-CXCR3 blocking antibody in the non-obese diabetic (NOD) mouse model of Sjögren’s syndrome (SS) to elucidate whether the interaction between CXCR3 and its ligands is required for the development of SS. Treatment with anti-CXCR3 significantly improved salivary secretion and reduced the percentage of CXCR3+CD8 T and CXCR3+CD44+CD8 T cells in the submandibular glands (SMGs) and submandibular lymph nodes. Furthermore, SMG expression of the inflammatory factor TNF-α was diminished by anti-CXCR3 treatment, while the expression of tight junction protein claudin-1 and water channel protein aquaporin 5, crucial for normal salivary secretion, was enhanced (Zhou & Yu, 2018; PMID: 29348563). This antibody was used for an in vivo CXCR3 blockade experiment to assess its effect on tumor response to radiation therapy and immunotherapy. Additionally, it was used in flow cytometric analysis of tumor-infiltrating lymphocytes and single-cell suspensions from the spleen, blood, and lymph nodes to detect CXCR3 expression (Luo et al., 2019; PMID: 31506388).
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