Anti-Mouse CD183 (Clone CXCR3-173) – Purified in vivo GOLD™ Functional Grade

Clone CXCR3-173 is most commonly used in mice for in vivo neutralization of the CXCR3 receptor, thereby blocking CXCR3-mediated chemokine signaling to study immune cell migration and function in various disease models. The antibody is also widely used in flow cytometric analysis to characterize and quantify CXCR3-expressing cells in mouse tissues.

Essential in vivo applications include:

• Neutralizing CXCR3 Function: Administration of CXCR3-173 in vivo inhibits the interaction of CXCR3 with its ligands (notably blocking binding of CXCL10 and CXCL11, but not CXCL9), which disrupts chemotactic migration and immune cell trafficking.

• Modeling Disease Processes: By blocking CXCR3, researchers have examined its role in:

  • Immune cell migration—especially CD4 and CD8 T-cells, NK cells, and regulatory T cells—to sites of inflammation or tumors.
  • Transplantation studies—modulation of allograft rejection and immune responses in organ transplantation models.
  • Autoimmunity and inflammatory diseases—as CXCR3 is involved in recruiting T cells to inflamed tissues, neutralization can clarify its function in disease progression and pathogenesis.

• Therapeutic Candidate Evaluation: As a direct neutralizing antibody, CXCR3-173 has been used to assess the therapeutic potential of CXCR3 blockade in preclinical mouse models of cancer, autoimmunity, and transplantation.

Additional notes:

• The antibody is a hamster IgG targeting the native form of mouse CXCR3 and does not work for Western blotting.
• High-purity, low-endotoxin preparations (such as the Ultra-LEAF™ format) are typically used for sensitive in vivo applications to minimize immune artifacts.

Summary table:

In summary, in vivo applications of clone CXCR3-173 in mice are chiefly focused on blocking CXCR3 to interrogate its role in immune cell migration, disease pathogenesis, and therapeutic intervention models.

CXCR3-173 is most commonly used in combination with antibodies against T cell and NK cell markers, regulatory T cell markers, and sometimes modulatory agents like rapamycin to analyze immune cell subsets in various immunological studies, particularly focused on transplantation and immune modulation.

Commonly paired antibodies and proteins include:

• T cell markers: CD3, CD4, and CD8, to identify and analyze the major T cell populations and subsets.
• NK cell markers: NK1.1, to assess NK cells and their function.
• Regulatory T cell markers: CD25 and Foxp3, typically used together to identify regulatory T cells (Tregs).
• Activation/memory markers: CD44 and CD62L, to distinguish between naive, effector, and memory T cell populations.
• Other chemokine receptors: CCR5, CCR7, and occasionally others, to compare or distinguish between chemokine-mediated trafficking pathways.
• Immunomodulatory agents: Rapamycin, often used in combination with CXCR3-173 in transplantation or tolerance models to modulate immune responses.

CXCR3-173 is mostly used in flow cytometry for immunophenotyping, especially to track Th1 cells, effector/memory T cells, and T cell infiltration into tissues during inflammation or transplantation. The focus is often on mouse models, as CXCR3-173 is hamster-derived and specific to the murine receptor.

Additional details:

• CXCR3-173 also detects the receptor on CD4+ and CD8+ T cells, regulatory T cells, natural killer (NK) T cells, and a subset of NK cells.
• The combination with rapamycin (immunosuppressant) is well-documented for models of allograft survival.

In summary, when using CXCR3-173, the literature most often features it in multicolor flow cytometry panels including CD3, CD4, CD8, NK1.1, CD25, Foxp3, CD44, CD62L, and frequently in studies involving the immunomodulator rapamycin to dissect immune subset function in disease and transplantation models.

The key findings from scientific citations of clone CXCR3-173 center on its function as a non-depleting, function-blocking monoclonal antibody targeting mouse CXCR3, useful for dissecting the role of CXCR3 in immune cell recruitment and tissue injury, notably in transplantation, tumor immunology, and inflammatory disease models.

Essential findings:

• Expression detection: CXCR3-173 identifies native CXCR3 on primary memory CD4^+^ and CD8^+^ T cells, regulatory T cells (CD4^+^CD25^+^Foxp3^+^), natural killer T (NKT) cells, and ~25% of NK cells.
• Functional blockade: In vitro, CXCR3-173 blocks chemotaxis in response to CXCL10 and CXCL11 but not CXCL9, distinguishing ligand-specific signaling mechanisms.
• Transplant survival: In vivo administration of CXCR3-173 significantly prolongs cardiac and islet allograft survival in mice. When combined with low-dose rapamycin, it can induce long-term (>100 days) graft survival.
• Non-depleting properties: Unlike earlier antibodies (e.g., depleting IgM anti-CXCR3), CXCR3-173 does not reduce the number of effector CD4^+^ T cells, allowing for mechanistic studies on CXCR3-dependent immune responses without altering the size of critical T cell pools.
• Disease models: CXCR3 blockade with CXCR3-173 mitigates immune-mediated lung pathology during viral infection without impairing viral clearance, demonstrating its importance in reducing tissue injury while preserving host defense.
• Immunotherapeutic potential: The antibody is valued for preclinical studies to probe CXCR3-driven inflammation and is suggested for developing strategies to inhibit immune-mediated rejection and inflammatory diseases in mice.

Additional technical notes:

• Not suitable for Western blotting: CXCR3-173 recognizes the native conformation and is ineffective in denatured-protein assays, but is highly useful in flow cytometry and functional blockade studies.
• Production: Generated by immunizing hamsters with a specific mouse CXCR3 peptide, validated by staining and in vitro/in vivo blockade assays.
• Coverage: Widely referenced in transplantation, autoimmunity, infection, and tumor immunology literature for its accuracy and reliability in characterizing CXCR3 function.

In summary, CXCR3-173 is the gold standard antibody for functionally interrogating mouse CXCR3 in vivo and in vitro, and is frequently cited for its ability to elucidate the receptor’s role in immune cell trafficking, tissue injury, and therapeutic intervention.

Dosing regimens of clone CXCR3-173 vary substantially across different mouse models depending on the disease context, experimental objectives, and treatment duration. The antibody has been employed in multiple therapeutic settings with markedly different administration protocols.

Transplantation and Allograft Models

In cardiac and islet allograft studies, CXCR3-173 was administered at doses ranging from 40 μg to 1 mg per mouse. The standard approach involved a single dose of 40 μg, with higher doses (200 μg and 1 mg) tested to evaluate dose-dependent effects without causing CD4+ T cell depletion. These treatments successfully prolonged allograft survival, and when combined with low-dose rapamycin, resulted in long-term survival of both cardiac and islet allografts.

Autoimmune Diabetes Models

The dosing strategies differ considerably in type 1 diabetes models. In RIP-LCMV-GP mice, CXCR3-173 was administered following three daily doses of anti-CD3 antibody (3 μg/day on Days 10-12 after LCMV infection). The CXCR3-173 treatment then followed in two distinct regimens: an acute treatment period (Days 13-28) or a chronic treatment protocol (Days 13-84). The chronic combination therapy achieved an impressive 82% disease remission rate compared to 42% with anti-CD3 monotherapy.

In NOD mice with recent-onset diabetes, treatment was initiated within one week of diabetes onset and continued for at least 10 weeks. This extended treatment protocol resulted in a 71% diabetes remission rate when CXCR3-173 was combined with anti-CD3, compared to 38% with anti-CD3 alone.

Kinetic and Mechanistic Studies

For kinetic experiments examining immune cell dynamics, C57BL/6 mice received the antibody treatment following a different schedule. Blood samples were collected at multiple time points (2, 24, and 48 hours, then at 6, 9, 13, 16, 22, and 27 days after the last injection) to track CXCR3 expression on various immune cell populations.

Other Disease Models

In tumor microenvironment studies, CXCR3-173 was administered via intraperitoneal injection at doses of 100, 200, and 500 μg, given once every other day for 2 weeks. This dosing schedule reflects an intermediate-intensity approach suitable for chronic inflammatory conditions.

The variation in these regimens reflects the biological context of each model: transplantation studies often use single or limited doses to prevent acute rejection, while autoimmune disease models require prolonged treatment to maintain remission and preserve tissue function. The flexibility in dosing demonstrates the antibody's utility across diverse experimental paradigms.