InVivoMAb anti-mouse Podoplanin (gp38)
Product Description
Specifications
| Isotype | Syrian hamster IgG |
|---|---|
| Recommended Isotype Control(s) | InVivoMAb polyclonal Syrian hamster IgG |
| Recommended Dilution Buffer | InVivoPure pH 7.0 Dilution Buffer |
| Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
| Immunogen | Mouse tymic epithelial cells |
| Reported Applications |
in vivo PDPN blockade in vitro PDPN blockade Immunofluorescence Western blot Flow cytometry |
| 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_2687718 |
| 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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Rouhani, S. J., et al (2015). "Roles of lymphatic endothelial cells expressing peripheral tissue antigens in CD4 T-cell tolerance induction" Nat Commun 6: 6771.
PubMed
Lymphatic endothelial cells (LECs) directly express peripheral tissue antigens and induce CD8 T-cell deletional tolerance. LECs express MHC-II molecules, suggesting they might also tolerize CD4 T cells. We demonstrate that when beta-galactosidase (beta-gal) is expressed in LECs, beta-gal-specific CD8 T cells undergo deletion via the PD-1/PD-L1 and LAG-3/MHC-II pathways. In contrast, LECs do not present endogenous beta-gal in the context of MHC-II molecules to beta-gal-specific CD4 T cells. Lack of presentation is independent of antigen localization, as membrane-bound haemagglutinin and I-Ealpha are also not presented by MHC-II molecules. LECs express invariant chain and cathepsin L, but not H2-M, suggesting that they cannot load endogenous antigenic peptides onto MHC-II molecules. Importantly, LECs transfer beta-gal to dendritic cells, which subsequently present it to induce CD4 T-cell anergy. Therefore, LECs serve as an antigen reservoir for CD4 T-cell tolerance, and MHC-II molecules on LECs are used to induce CD8 T-cell tolerance via LAG-3.
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Astarita, J. L., et al (2015). "The CLEC-2-podoplanin axis controls the contractility of fibroblastic reticular cells and lymph node microarchitecture" Nat Immunol 16(1): 75-84.
PubMed
In lymph nodes, fibroblastic reticular cells (FRCs) form a collagen-based reticular network that supports migratory dendritic cells (DCs) and T cells and transports lymph. A hallmark of FRCs is their propensity to contract collagen, yet this function is poorly understood. Here we demonstrate that podoplanin (PDPN) regulates actomyosin contractility in FRCs. Under resting conditions, when FRCs are unlikely to encounter mature DCs expressing the PDPN receptor CLEC-2, PDPN endowed FRCs with contractile function and exerted tension within the reticulum. Upon inflammation, CLEC-2 on mature DCs potently attenuated PDPN-mediated contractility, which resulted in FRC relaxation and reduced tissue stiffness. Disrupting PDPN function altered the homeostasis and spacing of FRCs and T cells, which resulted in an expanded reticular network and enhanced immunity.
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Dubrot, J., et al (2014). "Lymph node stromal cells acquire peptide-MHCII complexes from dendritic cells and induce antigen-specific CD4(+) T cell tolerance" J Exp Med 211(6): 1153-1166.
PubMed
Dendritic cells (DCs), and more recently lymph node stromal cells (LNSCs), have been described to tolerize self-reactive CD8(+) T cells in LNs. Although LNSCs express MHCII, it is unknown whether they can also impact CD4(+) T cell functions. We show that the promoter IV (pIV) of class II transactivator (CIITA), the master regulator of MHCII expression, controls endogenous MHCII expression by LNSCs. Unexpectedly, LNSCs also acquire peptide-MHCII complexes from DCs and induce CD4(+) T cell dysfunction by presenting transferred complexes to naive CD4(+) T cells and preventing their proliferation and survival. Our data reveals a novel, alternative mechanism where LN-resident stromal cells tolerize CD4(+) T cells through the presentation of self-antigens via transferred peptide-MHCII complexes of DC origin.
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Fleige, H., et al (2014). "IL-17-induced CXCL12 recruits B cells and induces follicle formation in BALT in the absence of differentiated FDCs" J Exp Med 211(4): 643-651.
PubMed
Ectopic lymphoid tissue, such as bronchus-associated lymphoid tissue (BALT) in the lung, develops spontaneously at sites of chronic inflammation or during infection. The molecular mechanisms underlying the neogenesis of such tertiary lymphoid tissue are still poorly understood. We show that the type of inflammation-inducing pathogen determines which key factors are required for the formation and maturation of BALT. Thus, a single intranasal administration of the poxvirus modified vaccinia virus Ankara (MVA) is sufficient to induce highly organized BALT with densely packed B cell follicles containing a network of CXCL13-expressing follicular DCs (FDCs), as well as CXCL12-producing follicular stromal cells. In contrast, mice treated with P. aeruginosa (P.a.) develop BALT but B cell follicles lack FDCs while still harboring CXCL12-positive follicular stromal cells. Furthermore, in IL-17-deficient mice, P.a.-induced BALT largely lacks B cells as well as CXCL12-expressing stromal cells, and only loose infiltrates of T cells are present. We show that Toll-like receptor pathways are required for BALT induction by P.a., but not MVA, and provide evidence that IL-17 drives the differentiation of lung stroma toward podoplanin-positive CXCL12-expressing cells that allow follicle formation even in the absence of FDCs. Taken together, our results identify distinct pathogen-dependent induction and maturation pathways for BALT formation.
Product Citations
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The perinecrotic niche of glioblastoma drives tumor-associated macrophage polarization and immunosuppression via podoplanin-mediated CLEC5A activation.
In J Clin Invest on 15 July 2026 by Li, J., Wang, X., et al.
PubMed
Glioblastoma (GBM), isocitrate dehydrogenase-WT (IDH-WT) (WHO grade 4) is the most common malignant glioma in adults and is characterized by a hypoxic and immunosuppressive tumor microenvironment (TME). Bone marrow-derived tumor-associated macrophages (TAMs) dominate the immune landscape in GBM and are recruited to the perinecrotic niche following the onset of necrosis. C-type lectin domain-containing 5A (CLEC5A) has the strongest association with poor clinical outcomes among immune-related genes in GBM and is preferentially expressed in hypoxic, perinecrotic TAMs. CLEC5A overexpression promotes TAM polarization toward an immunosuppressive phenotype and secretion of immunoregulatory cytokines. Using the replication-competent avian sarcoma-leukosis virus long terminal repeat with a splice acceptor (RCAS)/tumor virus A (tv-a) system GBM model with bone marrow transplantation from Clec5a-/- donor mice, we demonstrated that CLEC5A loss prolonged survival, delayed tumor progression, and attenuated TME immunosuppression. Mechanistically, podoplanin (PDPN) expressed on glioma cells directly engaged CLEC5A and triggered downstream Syk/JAK/STAT3 signaling in TAMs. Pharmacologic Syk inhibition suppressed glioma growth, diminished TAM infiltration and polarization, reversed the immunosuppressive TME, and prolonged survival in vivo. Collectively, our findings indicate that the PDPN/CLEC5A/Syk/STAT3 axis orchestrates TAM polarization and TME immunosuppression in the perinecrotic niche of GBM, highlighting CLEC5A/Syk as a promising therapeutic target for reversing the immunosuppressive TME and improving outcomes.
-
The perinecrotic niche of glioblastoma drives tumor-associated macrophage polarization and immunosuppression via podoplanin-mediated CLEC5A activation.
In J Clin Invest on 15 July 2026 by Li, J., Wang, X., et al.
PubMed
Glioblastoma (GBM), isocitrate dehydrogenase-WT (IDH-WT) (WHO grade 4) is the most common malignant glioma in adults and is characterized by a hypoxic and immunosuppressive tumor microenvironment (TME). Bone marrow-derived tumor-associated macrophages (TAMs) dominate the immune landscape in GBM and are recruited to the perinecrotic niche following the onset of necrosis. C-type lectin domain-containing 5A (CLEC5A) has the strongest association with poor clinical outcomes among immune-related genes in GBM and is preferentially expressed in hypoxic, perinecrotic TAMs. CLEC5A overexpression promotes TAM polarization toward an immunosuppressive phenotype and secretion of immunoregulatory cytokines. Using the replication-competent avian sarcoma-leukosis virus long terminal repeat with a splice acceptor (RCAS)/tumor virus A (tv-a) system GBM model with bone marrow transplantation from Clec5a-/- donor mice, we demonstrated that CLEC5A loss prolonged survival, delayed tumor progression, and attenuated TME immunosuppression. Mechanistically, podoplanin (PDPN) expressed on glioma cells directly engaged CLEC5A and triggered downstream Syk/JAK/STAT3 signaling in TAMs. Pharmacologic Syk inhibition suppressed glioma growth, diminished TAM infiltration and polarization, reversed the immunosuppressive TME, and prolonged survival in vivo. Collectively, our findings indicate that the PDPN/CLEC5A/Syk/STAT3 axis orchestrates TAM polarization and TME immunosuppression in the perinecrotic niche of GBM, highlighting CLEC5A/Syk as a promising therapeutic target for reversing the immunosuppressive TME and improving outcomes.
-
The perinecrotic niche of glioblastoma drives tumor-associated macrophage polarization and immunosuppression via podoplanin-mediated CLEC5A activation.
In J Clin Invest on 15 July 2026 by Li, J., Wang, X., et al.
PubMed
Glioblastoma (GBM), isocitrate dehydrogenase-WT (IDH-WT) (WHO grade 4) is the most common malignant glioma in adults and is characterized by a hypoxic and immunosuppressive tumor microenvironment (TME). Bone marrow-derived tumor-associated macrophages (TAMs) dominate the immune landscape in GBM and are recruited to the perinecrotic niche following the onset of necrosis. C-type lectin domain-containing 5A (CLEC5A) has the strongest association with poor clinical outcomes among immune-related genes in GBM and is preferentially expressed in hypoxic, perinecrotic TAMs. CLEC5A overexpression promotes TAM polarization toward an immunosuppressive phenotype and secretion of immunoregulatory cytokines. Using the replication-competent avian sarcoma-leukosis virus long terminal repeat with a splice acceptor (RCAS)/tumor virus A (tv-a) system GBM model with bone marrow transplantation from Clec5a-/- donor mice, we demonstrated that CLEC5A loss prolonged survival, delayed tumor progression, and attenuated TME immunosuppression. Mechanistically, podoplanin (PDPN) expressed on glioma cells directly engaged CLEC5A and triggered downstream Syk/JAK/STAT3 signaling in TAMs. Pharmacologic Syk inhibition suppressed glioma growth, diminished TAM infiltration and polarization, reversed the immunosuppressive TME, and prolonged survival in vivo. Collectively, our findings indicate that the PDPN/CLEC5A/Syk/STAT3 axis orchestrates TAM polarization and TME immunosuppression in the perinecrotic niche of GBM, highlighting CLEC5A/Syk as a promising therapeutic target for reversing the immunosuppressive TME and improving outcomes.
-
The perinecrotic niche of glioblastoma drives tumor-associated macrophage polarization and immunosuppression via podoplanin-mediated CLEC5A activation.
In J Clin Invest on 15 July 2026 by Li, J., Wang, X., et al.
PubMed
Glioblastoma (GBM), isocitrate dehydrogenase-WT (IDH-WT) (WHO grade 4) is the most common malignant glioma in adults and is characterized by a hypoxic and immunosuppressive tumor microenvironment (TME). Bone marrow-derived tumor-associated macrophages (TAMs) dominate the immune landscape in GBM and are recruited to the perinecrotic niche following the onset of necrosis. C-type lectin domain-containing 5A (CLEC5A) has the strongest association with poor clinical outcomes among immune-related genes in GBM and is preferentially expressed in hypoxic, perinecrotic TAMs. CLEC5A overexpression promotes TAM polarization toward an immunosuppressive phenotype and secretion of immunoregulatory cytokines. Using the replication-competent avian sarcoma-leukosis virus long terminal repeat with a splice acceptor (RCAS)/tumor virus A (tv-a) system GBM model with bone marrow transplantation from Clec5a-/- donor mice, we demonstrated that CLEC5A loss prolonged survival, delayed tumor progression, and attenuated TME immunosuppression. Mechanistically, podoplanin (PDPN) expressed on glioma cells directly engaged CLEC5A and triggered downstream Syk/JAK/STAT3 signaling in TAMs. Pharmacologic Syk inhibition suppressed glioma growth, diminished TAM infiltration and polarization, reversed the immunosuppressive TME, and prolonged survival in vivo. Collectively, our findings indicate that the PDPN/CLEC5A/Syk/STAT3 axis orchestrates TAM polarization and TME immunosuppression in the perinecrotic niche of GBM, highlighting CLEC5A/Syk as a promising therapeutic target for reversing the immunosuppressive TME and improving outcomes.