anti-V-Set and Immunoglobulin Domain-Containing Protein 4 (VSIG4) Antikörper

Human V-Set and Immunoglobulin Domain-Containing Protein 4 (VSIG4) Interaktionspartner

1. this study shows that CRIg/FH ameliorates renal ischemia reperfusion injury via activation of PI3K/AKT signaling

2. CRIg is a novel interacting partner of TRIM72 in the lung.

3. Soluble VSIG4 levels are associated with the progression and recurrence of ovarian cancer, indicating that soluble VSIG4 may be used as a potential biomarker for predicting tumor prognosis.

4. VSIG4 signaling provides an anti-immune evasion mechanism that prevents the outgrowth of intracellular bacteria in macrophages

5. The VSIG4 upregulation by LMP1 was regulated at the transcriptional level via the NF-kB signaling axis.

6. VSIG4 expression is significantly upregulated in human masticatory mucosa during wound healing

7. we concluded that let-7g-5p inhibits epithelial-mesenchymal transition (EMT) consistent with reduction of glioma stem cell (GSC) phenotypes by targeting VSIG4 in glioblastoma.

8. Data indicate that rotein kinase calpha (PKCalpha) plays a role in downregulating complement receptor Ig (CRIg coded by V-set and Ig domain-containing protein 4 VSIG4) expression.

9. complement receptor of the immunoglobulin superfamily-L-factor H protects glomerular mesangial cells from complement-mediated injury and proliferative lesions

10. we identified VSIG4 as a potential diagnostic marker of severe preeclampsia. The determination of this gene may improve the prognostic assessment of severe preeclampsia.

11. Data indicate that massive V-set and Ig domain-containing 4 VSIG4(+) cell infiltration throughout the non-small-cell lung cancer samples.

12. we showed that a complement receptor of the Ig superfamily (CRIg, also known as Z39Ig), a receptor for complement fragments (C3b and iC3b), was expressed on a subset of intestinal macrophages in murine and human large intestine

13. These results suggest that T cells can opposite T cell hyporesponsiveness through dampening Z39Ig inhibitory signals from macrophages and thus maintain their anti-viral function in chronic hepatitis B.

14. hVSIG4 recombinant adenovirus-transfected DCs suppress T cell proliferation, cytokine production and activation marker expression with

15. Results report the identification and characterization of a Complement Receptor of the Immunoglobulin superfamily, CRIg, that binds complement fragments C3b and iC3b.

16. These data indicate that the macrophage Z39Ig is involved in the pathogenesis of inflammatory diseases through chemokine induction, which will promote the migration of inflammatory cells into the lesion area, and MMP-9 induction.

17. The specific expression of VSIG4 on resting macrophages suggests that VSIG4 may be important for the maintenance of T cell unresponsiveness in healthy tissues.

18. CRIg is not only a phagocytic receptor, but also a potent inhibitor of the alternative pathway convertases

Mouse (Murine) V-Set and Immunoglobulin Domain-Containing Protein 4 (VSIG4) Interaktionspartner

1. CRIg expression in the lung and its role in the lung innate immunity.

2. Kupffer cells play a critical role in inducing regulatory T cells and establishing immune tolerance against oral antigens via VSIG4 signaling.

3. VSIG4 activates the PI3K/Akt-STAT3 pathway, leading to pyruvate dehydrogenase kinase-2 (PDK2) upregulation and subsequent phosphorylation of pyruvate dehydrogenase, which results in reduction in pyruvate/acetyl-CoA conversion, mitochondrial reactive oxygen species secretion, and macrophage inhibition.

4. Thus, environmental cues instruct tissue-resident macrophages to express CRIg, which functions as an immune checkpoint molecule to regulate adaptive immunity and promote immune tolerance.

5. VSIG4 signaling provides an anti-immune evasion mechanism that prevents the outgrowth of intracellular bacteria in macrophages

6. These findings reveal a pattern recognition role for CRIg in the direct capture of circulating Gram-positive bacteria from the bloodstream via binding to bacterial teichoic acid.

7. plays a negative role in helper T cell-dependent antibody isotype switching

8. The macrophage-expressed VSIG4 may act to alleviate renal tubulointerstitial injury via inhibition of T cell infiltration and secretion of inflammation related factors.

9. complement receptor of the immunoglobulin superfamily-L-factor H protects glomerular mesangial cells from complement-mediated injury and proliferative lesions

10. CRIg signals induce anti-intracellular bacterial phagosome activity in a chloride intracellular channel 3-dependent manner.

11. CRIg plays an important role in regulating virus-induced Kupffer cell death and depletion of these cells from the liver sinusoidal lumen

12. we showed that a complement receptor of the Ig superfamily (CRIg, also known as Z39Ig), a receptor for complement fragments (C3b and iC3b), was expressed on a subset of intestinal macrophages in murine and human large intestine

13. The interstitial inflammatory cell infiltration and tubular lesion of VSIG4(-/-); urethral obstruction operation mice were increased, with the expression of TGF-beta1 increased and MMP-2 reduced. VSIG4 may play a role in inhibiting interstitial fibrosis.

14. Results report the identification and characterization of a Complement Receptor of the Immunoglobulin superfamily, CRIg, that binds complement fragments C3b and iC3b.

15. The specific expression of VSIG4 on resting macrophages suggests that VSIG4 may be important for the maintenance of T cell unresponsiveness in healthy tissues.

16. A soluble form of complement receptor of the immunoglobulin superfamily (CRIg) reversed inflammation and bone loss in two experimental models of arthritis by inhibiting the alternative pathway of complement in the joint.

17. Antibody blocking or gene ablation of the newly identified complement receptor CRIg, but not complement receptor 3 (CR3), rescued DAF/Crry-deficient platelets from complement-dependent elimination.

18. CRIg thus identifies a subset of tissue resident macrophages capable of increased phagocytosis of complement C3-coated particles, a function critical for immune clearance