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

Clone CXCR3-173 is commonly used in vivo in mice primarily as a neutralizing (blocking) monoclonal antibody targeting the chemokine receptor CXCR3 (CD183), which is expressed on subsets of T cells and NK cells. Its most well-established in vivo applications are as follows:

• Blockade of CXCR3-mediated chemotaxis and cell trafficking: CXCR3-173 prevents chemokine-driven recruitment of activated T cells (especially Th1-type and effector/memory T cells), regulatory T cells (Tregs), and NK cells to inflamed sites or transplanted tissues.
• Inhibition of immune responses in transplantation models: It is frequently employed to prolong allograft survival in models such as cardiac and islet transplantation by blocking T cell infiltration into grafts.
• Immunomodulation in inflammatory and autoimmune disease models: Due to its ability to disrupt CXCR3-driven trafficking of immune cells, CXCR3-173 is used to investigate and ameliorate pathological T cell responses in vivo, particularly those involving type 1 immunity.

Key details on mechanism and use:

• CXCR3-173 recognizes the native, surface-expressed form of CXCR3 on mouse cells. It does not work in denatured protein assays such as Western blotting.
• In vivo, the antibody effectively blocks migration and accumulation of T cells in response to CXCL10 or CXCL11, but not CXCL9.
• Shown to synergize with immunosuppressive drugs such as rapamycin to further enhance graft survival.

Other experimental applications:

• Used for in vivo depletion or blockade experiments to study the role of CXCR3+ cells in immunopathology, tumor immunity, autoimmune disease, and infectious disease models.
• Applied in immune cell trafficking studies, often combined with flow cytometric analysis to assess blockade efficacy and immune cell phenotypes.

Summary Table: Common In Vivo Applications of CXCR3-173 in Mice

In summary, CXCR3-173 is a well-established tool for in vivo blockade of CXCR3 functions in mice, enabling mechanistic studies of immune cell recruitment and the development of therapeutic strategies in transplantation, autoimmunity, and tumor models.

Commonly used antibodies or proteins paired with CXCR3-173 in experimental literature primarily target cellular markers for the characterization and functional analysis of immune cell subsets, especially in the context of transplantation, inflammation, and immune modulation models.

Key antibodies and proteins frequently used with CXCR3-173 include:

• T cell markers: CD4, CD8
  Used to identify helper T cells (CD4(^+)) and cytotoxic T cells (CD8(^+)), as CXCR3 is expressed on memory phenotype CD4(^+) and CD8(^+) T cells.

• Regulatory T cell markers: CD25, Foxp3
  These define regulatory T cells (Tregs), which are a crucial CXCR3-expressing population.

• NK and NKT cell markers: NK1.1, CD49b, CD3
  NK and NKT cells are partially CXCR3-positive; these markers help distinguish their subsets in multiparametric analyses.

• Activation markers: CD44, CD69, CD62L
  These are often used to determine activation and memory status of T lymphocytes in conjunction with CXCR3 expression.

• Chemokines: CXCL9 (MIG), CXCL10 (IP-10), CXCL11 (I-TAC)
  These are functional ligands for CXCR3 and are used in chemotaxis assays or to probe receptor-blocking activity in vitro.

• Immunomodulatory agents: Rapamycin
  In vivo models often combine CXCR3-173 with rapamycin to study synergistic effects on transplantation tolerance and immunosuppression.

To summarize, the most commonly paired antibodies/proteins with CXCR3-173 in research are those recognizing lineage (CD4, CD8, NK1.1, CD3), regulatory (CD25, Foxp3), and activation/memory (CD44, CD69, CD62L) markers, as well as chemokine ligands and immunomodulators like rapamycin. This multi-marker approach allows for comprehensive immunophenotyping and mechanistic studies in murine immune models.

Clone CXCR3-173 is a well-characterized, non-depleting, function-blocking monoclonal antibody that specifically targets murine CXCR3, and it is widely cited in scientific literature for its critical role in dissecting CXCR3 function, particularly in immune cell trafficking, transplantation tolerance, tumor immunology, and models of inflammatory disease.

Key findings from CXCR3-173 citations include:

• CXCR3-173 specifically recognizes mouse CXCR3 on primary memory phenotype CD4+ and CD8+ T cells, CD4+CD25+ Foxp3+ regulatory T cells, natural killer (NK) T cells, and about 25% of NK cells.

• Functionally blocks CXCR3-mediated chemotaxis: In vitro, CXCR3-173 effectively inhibits chemotaxis of immune cells in response to the chemokines CXCL10 and CXCL11, but not to CXCL9.

• Prolongs allograft survival: In vivo, administration of CXCR3-173 significantly prolongs both cardiac and islet allograft survival in mice, a benefit further enhanced when combined with rapamycin, a commonly used immunosuppressant.

  • This prolongation occurs without depletion of effector lymphocytes—CXCR3-173 does not deplete CD4+ T cells or total splenocytes, which distinguishes it from older, depleting anti-CXCR3 antibodies.

• Utility in immunotherapy studies: CXCR3-173 has enabled in-depth analysis of CXCR3’s role in immune cell recruitment and tissue inflammation, making it a valuable research tool in transplantation, infection, and autoimmune models.

• Impact on infection models: CXCR3-173-mediated blockade during acute lung viral infections (e.g., influenza) reduces lung injury and disease severity, hastens resolution of inflammation, but does not impair viral clearance, suggesting a dissociation between immune-mediated pathology and normal antiviral defense.

• Technical features: CXCR3-173 recognizes the native, cell surface conformation of mouse CXCR3, but does not work in Western blotting; it is validated mainly for flow cytometry and in vivo functional assays.

• Key references in the literature: Some highly cited studies using CXCR3-173 include characterizations by Hancock et al. (J Exp Med, 2000/2001), Uppaluri et al. (Transplantation, 2008), and more recent works dissecting its function in viral immunopathology and chronic disease models.

In summary: Scientific literature consistently recognizes CXCR3-173 as a powerful, non-depleting, function-blocking antibody to dissect CXCR3’s role in immune cell trafficking—particularly to study mechanisms of transplant rejection, immune-mediated diseases, and tissue inflammation in mice. It is regarded as a gold-standard reagent for in vivo and ex vivo functional studies of murine CXCR3.

Dosing regimens for clone CXCR3-173 in mouse models vary based on the experimental purpose, mouse strain, and disease context, but typical doses range from 40 μg to 1 mg per mouse and are administered either as single or multiple intraperitoneal (i.p.) injections over periods from days to weeks.

• Cardiac & Islet Allograft Models (C57BL/6 Mice):

  • Single doses of 40 μg, 200 μg, or 1 mg CXCR3-173 mAb were used, with analyses typically performed 5 days post-injection to assess cellular responses without significant depletion of key immune subsets.
  • Repeated dosing regimens are sometimes employed in combination studies, particularly when used with immunosuppressants (e.g., rapamycin or cyclosporine), but the single-dose approach is common for characterizing immune modulation.

• Inflammation or Disease Mechanism Models (e.g., C57BL/6, H2d Mice):

  • Doses of 100 μg, 200 μg, or 500 μg via i.p. injection, administered once every other day for 2 weeks, are used to examine functional effects on chemokine signaling and immune cell migration.
  • Regimens may be tailored for acute versus chronic treatment, depending on whether the focus is on short-term blockade or longer-term disease modulation.

• General Observations:

  • Dose selection relates to the desired functional outcome—lower doses may suffice for flow cytometry or immunophenotyping, while higher or repeated doses are often necessary for functional blockade or therapeutic studies.
  • The interval and duration of dosing (single vs. repeated; daily vs. alternate days; duration of weeks) depend on disease progression and specific immune readouts.

• Neurofibroma and Other Disease Models:

  • Studies in NF1/neurofibroma used varying regimens but noted that therapeutic effects were not robust under tested protocols, highlighting the importance of disease-specific optimization.

In summary, the most common dosing pattern for CXCR3-173 in mice falls between 40 μg and 1 mg per dose, administered via intraperitoneal injection, with adjustments for dose frequency and total duration according to disease model and experimental goals. If you seek a specific disease context (autoimmunity, transplantation, inflammation), more tailored regimens may exist in specialized protocols.