InVivoMAb anti-mouse CXCL9 (MIG)
Product Description
Specifications
| Isotype | Armenian Hamster IgG, κ |
|---|---|
| Recommended Isotype Control(s) | InVivoMAb polyclonal Armenian hamster IgG |
| Recommended Dilution Buffer | InVivoPure pH 7.0 Dilution Buffer |
| Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
| Reported Applications |
in vivo CXCL9 neutralization Immunofluorescence |
| Formulation |
PBS, pH 7.0 Contains no stabilizers or preservatives |
| Endotoxin |
≤1EU/mg (≤0.001EU/μg) Determined by LAL assay |
| Purity |
≥95% Determined by SDS-PAGE |
| Sterility | 0.2 µm filtration |
| Production | Purified from cell culture supernatant in an animal-free facility |
| Purification | Protein A |
| RRID | AB_2736989 |
| Molecular Weight | 150 kDa |
| Storage | The antibody solution should be stored at the stock concentration at 4°C. Do not freeze. |
| Need a Custom Formulation? | See All Antibody Customization Options |
Application References
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Moreno-Fernandez, M. E., et al (2021). "PKM2-dependent metabolic skewing of hepatic Th17 cells regulates pathogenesis of non-alcoholic fatty liver disease" Cell Metab 33(6): 1187-1204 e1189.
PubMed
Emerging evidence suggests a key contribution to non-alcoholic fatty liver disease (NAFLD) pathogenesis by Th17 cells. The pathogenic characteristics and mechanisms of hepatic Th17 cells, however, remain unknown. Here, we uncover and characterize a distinct population of inflammatory hepatic CXCR3(+)Th17 (ihTh17) cells sufficient to exacerbate NAFLD pathogenesis. Hepatic ihTh17 cell accrual was dependent on the liver microenvironment and CXCR3 axis activation. Mechanistically, the pathogenic potential of ihTh17 cells correlated with increased chromatin accessibility, glycolytic output, and concomitant production of IL-17A, IFNgamma, and TNFalpha. Modulation of glycolysis using 2-DG or cell-specific PKM2 deletion was sufficient to reverse ihTh17-centric inflammatory vigor and NAFLD severity. Importantly, ihTh17 cell characteristics, CXCR3 axis activation, and hepatic expression of glycolytic genes were conserved in human NAFLD. Together, our data show that the steatotic liver microenvironment regulates Th17 cell accrual, metabolism, and competence toward an ihTh17 fate. Modulation of these pathways holds potential for development of novel therapeutic strategies for NAFLD.
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Wang, C., et al (2021). "Reprogramming NK cells and macrophages via combined antibody and cytokine therapy primes tumors for elimination by checkpoint blockade" Cell Rep 37(8): 110021.
PubMed
Treatments aiming to augment immune checkpoint blockade (ICB) in cancer often focus on T cell immunity, but innate immune cells may have important roles to play. Here, we demonstrate a single-dose combination treatment (termed AIP) using a pan-tumor-targeting antibody surrogate, half-life-extended interleukin-2 (IL-2), and anti-programmed cell death 1 (PD-1), which primes tumors to respond to subsequent ICB and promotes rejection of large established tumors in mice. Natural killer (NK) cells and macrophages activated by AIP treatment underwent transcriptional reprogramming; rapidly killed cancer cells; governed the recruitment of cross-presenting dendritic cells (DCs) and other leukocytes; and induced normalization of the tumor vasculature, facilitating further immune infiltration. Thus, innate cell-activating therapies can initiate critical steps leading to a self-sustaining cycle of T cell priming driven by ICB.
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Qu, Y., et al (2020). "Baseline Frequency of Inflammatory Cxcl9-Expressing Tumor-Associated Macrophages Predicts Response to Avelumab Treatment" Cell Rep 32(1): 107873.
PubMed
The tumor microenvironment is rich with immune-suppressive macrophages that are associated with cancer progression and resistance to immune checkpoint therapy. Using pre-treatment tumor biopsies complemented with single-cell RNA sequencing (RNA-seq), we characterize intratumoral immune heterogeneity to unveil potential mechanisms of resistance to avelumab (anti-PD-L1). We identify a proinflammatory F480(+)MHCII(+)Ly6C(lo) macrophage population that is associated with response rather than resistance to avelumab. These macrophages are the primary source of the interferon-inducible chemokine Cxcl9, which facilitates the recruitment of protective Cxcr3(+) T cells. Consequently, the efficacy of avelumab in mouse tumor models is dependent on Cxcr3 and Cxcl9, and baseline levels of Cxcl9 in patients treated with avelumab are associated with clinical response and overall survival. These data suggest that, within the broadly immune-suppressive macrophage compartment, a pro-inflammatory population exists that promotes responsiveness to PD-L1 blockade.
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Dangaj, D., et al (2019). "Cooperation between Constitutive and Inducible Chemokines Enables T Cell Engraftment and Immune Attack in Solid Tumors" Cancer Cell 35(6): 885-900 e810.
PubMed
We investigated the role of chemokines in regulating T cell accumulation in solid tumors. CCL5 and CXCL9 overexpression was associated with CD8(+) T cell infiltration in solid tumors. T cell infiltration required tumor cell-derived CCL5 and was amplified by IFN-gamma-inducible, myeloid cell-secreted CXCL9. CCL5 and CXCL9 coexpression revealed immunoreactive tumors with prolonged survival and response to checkpoint blockade. Loss of CCL5 expression in human tumors was associated with epigenetic silencing through DNA methylation. Reduction of CCL5 expression caused tumor-infiltrating lymphocyte (TIL) desertification, whereas forced CCL5 expression prevented Cxcl9 expression and TILs loss, and attenuated tumor growth in mice through IFN-gamma. The cooperation between tumor-derived CCL5 and IFN-gamma-inducible CXCR3 ligands secreted by myeloid cells is key for orchestrating T cell infiltration in immunoreactive and immunoresponsive tumors.
Product Citations
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Preoperative exercise induces anti-tumor Kupffer cells to prevent surgical stress-promoted colorectal cancer liver metastasis.
In Cell Rep Med on 17 February 2026 by Zhang, Y., Zhang, Y., et al.
PubMed
Colorectal cancer mortality is primarily driven by hepatic metastasis, with 50-60% of patients relapsing following liver metastasis resection due to micro-metastases or tumor cell dissemination. Surgery-induced immunologic disturbances contribute to liver recurrence. Exercise modulates immune responses, yet its role in surgical stress-promoted liver metastasis remains unclear. We demonstrate that 4 weeks of preoperative exercise (PEx) limits tumor growth in a murine model of surgical stress-promoted liver metastasis by shifting Kupffer cells toward an anti-tumor phenotype. PEx promotes Kupffer cell cytotoxic cytokines release and enhances CD8+ T cells recruitment and activation via the CXCL9-CXCR3 axis. Elevated CXCL9 levels are observed in murine and patient sera post exercise, with Kupffer cells identified as the primary source. Furthermore, exercise-induced butyrate accumulation in Kupffer cells inhibits histone deacetylase 3 activity, promoting CXCL9 expression. These findings suggest that PEx may serve as a non-invasive strategy to reduce recurrence and provide potential targets for exercise-mimetic therapies.
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Intravascular immune surveillance against viremia requires spatiotemporal coordination between Kupffer cells and ILC1s.
In Cell Rep on 25 November 2025 by Zhang, Q., Li, L., et al.
PubMed
Prompt sequestration and clearance of circulating virions by the liver are crucial for mitigating viral pathogenesis, yet the underlying immune mechanisms remain incompletely understood. Using real-time intravital imaging, here we reveal a tissue-specific behavioral adaptation of ILC1s that fortifies Kupffer cell (KC)-mediated intravascular immunosurveillance against viremia. At steady state, ILC1s constantly patrol and scan over KCs in liver sinusoids. Upon bloodstream infection with murine cytomegalovirus (MCMV) or vesicular stomatitis virus (VSV), KCs rapidly capture virions and trigger type I interferon production, which signals ILC1s to dock on infected KCs and undergo activation. Interferon-γ derived from arrested ILC1s facilitates viral clearance within KCs via an inducible nitric oxide synthase (iNOS)-NO-dependent mechanism. Impaired viral control in KCs, due to the absence of ILC1s, interferon-γ, or iNOS, leads to KC lysis and viral dissemination. Our study thus highlights a spatiotemporally coordinated defensive strategy between sessile and mobile tissue-resident immune sentinels in restraining viral infections.
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Targeting fibroblast derived thrombospondin 2 disrupts an immune-exclusionary environment at the tumor front in colorectal cancer.
In Nat Commun on 23 November 2025 by Iwane, K., Nakanishi, Y., et al.
PubMed
Fibrotic colorectal cancers (CRC) are largely microsatellite-stable and display desmoplastic stroma with poor immune infiltration. Here we identify thrombospondin-2 (THBS2) as a key regulator of the immune-exclusionary phenotype in fibrotic CRC. THBS2 is highly expressed by matrix cancer-associated fibroblasts at the tumor front. In an orthotopic model using desmoplastic tumor organoids, global or fibroblast-specific Thbs2 deletion disrupts the exclusionary barrier and increases intratumoral CD8 T cells. Mechanistically, THBS2 limits recruitment of CXCR3+ CD8 T cells by restraining dendritic- and macrophage-derived CXCL9/10. Depletion of these myeloid cells or blockade of CXCL9/10-CXCR3 signaling abolishes the enhanced CD8 T-cell influx and antitumor efficacy. Spatial profiling demonstrates that THBS2 loss induces proximity between CD8 T cells and myeloid cells and upregulates chemokines. Despite increased infiltration, CD8 T cells manifest exhaustion, rendering tumors highly susceptible to immune checkpoint blockade. THBS2 thus represents a tractable CAF-restricted target to overcome immune exclusion in fibrotic CRCs.
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Cxcl9high macrophages recruit circulating Cxcr3+ plasmablasts into kidneys to promote pathogenesis of lupus nephritis mice.
In Commun Biol on 9 October 2025 by Zhao, J., Bai, X., et al.
PubMed
Systemic lupus erythematosus (SLE) is an autoimmune disease driven by autoantibody production. Lupus nephritis (LN), a severe SLE complication, is primarily caused by renal autoantibodies. Long-lived plasma cells (LLPCs), the main producers of these autoantibodies, are especially elevated in the kidney of LN patients, particularly in refractory or recurrent cases. However, the cause of increased LLPCs in LN kidneys remains unknown. This study uses an LN mouse model and combines single-cell RNA sequencing with spatial transcriptomics, finding that kidney-resident Cxcl9high macrophages and their secreted chemokine Cxcl9 significantly rise with disease progression. This increase in Cxcl9 attracts Cxcr3+ plasmablasts in peripheral blood into the kidneys, where they differentiate into LLPCs and produce autoantibodies. Based on these findings, this study suggests that Cxcl9high macrophages are the inducing factor causing the increase of LLPCs in LN kidneys and may be a potential therapeutic target for LN.