Browse our anti-Integrin, alpha X (Complement Component 3 Receptor 4 Subunit) (ITGAX) Antibodies

Human Integrin, alpha X (Complement Component 3 Receptor 4 Subunit) (ITGAX) interaction partners

1. results suggested that ITGAX and ITGAM gene polymorphisms were associated with IgA nephropathy (IgAN) in a Chinese Han population, and the rs11150619-T allele showed a potential protective role for IgAN.

2. We demonstrated a strong correlation of CD11c expression, which represents dendritic cells (DCs) , with Tumor-infiltrating lymphocytes (TILs) and TLSs in triple-negative breast cancer (TNBC). Further investigation is warranted to identify therapeutic modalities that facilitate recruitment and activation of DCs.

3. This study provides evidence that CD11c is involved in the susceptibility to Behcet's disease in a Chinese Han population.

4. The main mechanism of Integrin alphaXbeta2 I-domain binding to RAGE is a charge interaction, in which the acidic moieties of Integrin alphaXbeta2 I-domains, including E244, and D249, recognize the basic residues on the RAGE V-domain encompassing K39, K43, K44, R104, and K107.

5. Studies indicate that CD11c+ T-bet+ memory B cells exhibit a distinct transcriptome.

6. Studies indicate enriched expression of TBX21 (T-bet), which is important for B cell survival and response to antigen, was observed in CD11c+ B cells.

7. CD11c, expressed not only in Hairy cell leukemia but also in dendritic cells, macrophages and monocytes is a differentiation marker for inflammation. Prolonged inflammation in the microenvironment of CLL cells may cause a susceptibility to autoimmune disorders and secondary tumors in CLL, in this way, an increase in mortality.

8. We can achieve possible clinical significance of lymphoma tumor microenvironments through CD11c and FOXP3 immunohistochemistry stains in extranodal diffuse large B-cell lymphoma patients receiving R-CHOP therapy.

9. Circulating CD11c+ T cells were associated with the expression of multiple adhesion molecules in women, suggesting that these cells have high tissue homing potential. These data suggest that CD11c expression distinguishes a population of circulating T cells during bacterial infection with innate capacity and mucosal homing potential.

10. CD8+ T cells of Behcet's disease patients exhibited increased CD11c expression levels, which may contribute to disease pathogenesis.

11. High expression of CD11c decreased the risk of death and relapse, and may be regarded as an alternative indicator of favorable prognosis in patients with gastric cancer.

12. the CD11c molecule possesses four different cellular patterns in the periprosthetic tissues.

13. Data show that secreted aspartic protease 2 (Sap2) of Candida albicans inactivates human macrophage complement factor H (factor H), factor H-receptors CD11b/CD18 and CD11c/CD18.

14. Data show that the percentage of CD11c positive antigen presenting cells (CD11c(+) APCs) in the peripheral blood of active pulmonary tuberculosis (APT) patients was much higher than that in the controls.

15. Data suggest that blood neutrophils expressing CD11c antigen and EMR2 protein be considered as potential biomarkers for sepsis and systemic inflammatory response syndrome (SIRS), respectively.

16. Modification of Levels of Adhesion Molecule Expression of Human Innate Immune Cells by Glycopolymers of Marine Bacteria

17. beta2 integrins-mediated chemosensory adhesion and migration of polymorphonuclear leukocytes on the vascular graft surface, bacterial cellulose.

18. three of these five genes (CXCL14, ITGAX, and LPCAT2) harbored polymorphisms associated with aggressive disease development in a human GWAS cohort consisting of 1,172 prostate cancer patients.

19. infiltration of MBP(+) and CD11c(+) innate immune cells show a significant association with phenotype and disease extent of non-asthmatic chronic rhinosinusitis

20. CD11a, CD11c, and CD18 gene polymorphisms and susceptibility to Behcet's disease in Koreans.

Mouse (Murine) Integrin, alpha X (Complement Component 3 Receptor 4 Subunit) (ITGAX) interaction partners

1. We suggest that targeted depletion of CD11c(+) cells associated with the islet vasculature may yield a therapeutic target to inhibit T cell trafficking to inflamed islets to prevent progression of type 1 diabetes.

2. findings imply that CD11c-positive microglia can potentially counteract amyloid deposition via increased Abeta-uptake and degradation, and by containing the inflammatory response.

3. High-fat diet -induced TLR4 activation inhibited macrophage proliferation, leading to greater accumulation of recruited CD11c(+) adipose tissue macrophages.

4. CD11c and its partner Itgb2 were required for DC capture of CD47-deficient cells. CD11b was not necessary for this process but could partially compensate in the absence of CD11c. Mice with DCs lacking Talin1, Itgb2, or CD11c were defective in supporting T-cell proliferation and differentiation induced by CD47-deficient cell associated antigen.

5. alphaXbeta2 uses the alphaX alphaI domain to bind iC3b on its C3c moiety at one of two sites.

6. Deleting IL-2 in CD11c(high)MHCII(+) cells induces spontaneous colitis resembling human inflammatory bowel disease.

7. Accumulation of lung CD11c+ DCs is significantly higher in both inflammatory and fibrotic phases of the disease but that percentages got reduced in the absence of TGF-beta.

8. The findings of this study indicate that radio-resistant cells, expressing CD11c-GFP+ and located in the CNS, irrespective of their origin, which might be the yolk sac or the periphery, show a phenotype capable of antigen presentation under neuroinflammatory conditions following induction of EAE.

9. These data demonstrated that the CD11c+ lamina propria mononuclear phagocytes from this postinfectious irritable bowel syndrome mouse model were not only able to transfer enteric inflammation to the normal mice but also caused abnormal intestinal function, characterized by epithelial barrier disruption and visceral hyperalgesia.

10. the CD11c promoter was unexpectedly active and triggered Mgat2 deletion within multiple hematopoietic lineages, showed remarkably poor penetrance within native DC populations, and produced almost undetectable levels of green fluorescent protein signal. These findings show that the CD11c promoter is not DC-specific, and extreme care should be taken in the interpretation of data using any mouse created using the CD11c-CRE

11. Studies indicate that the autoimmune phenotype in DEF6 and SWAP-70 knock-out (DKO) mice is characterized by the accumulation of B cell subset that expresses high levels of CD11c and T-bet (ABCs).

12. MyD88 signaling in lysozyme M and CD11c-expressing myeloid cells, as well as in pulmonary epithelial cells, is critical to restore inflammatory cytokine and antimicrobial peptide production, leading to efficient neutrophil recruitment and enhanced bacterial clearance.

13. Results implicate a monocytic origin of CD11c(+) cells in inflamed islets and suggest that therapeutic regulatory T cells directly or indirectly regulate their influx by altering the chemotactic milieu in the islets.

14. this study shows that PU.1 functions as a positive regulator of CD11c gene expression by directly binding to the Itgax promoter and through transactivation of the Irf4 gene

15. Murine CD11c+ T cells analyzed by flow cytometry display markers associated with non-conventional T cell subsets, including gammadelta T cells and invariant natural killer T (iNKT) cells.

16. Data concluded that the ablation of CD11c(hi) dendritic cells provided a subsidiary impact on blood-brain barrier (BBB) integrity and the expression of tight junction/adhesion molecules, thereby leading to exacerbated Japanese encephalitis (JE) progression.

17. CD11c(+) monocyte/macrophages promote chronic Helicobacter hepaticus-induced intestinal inflammation through the production of IL-23.

18. data demonstrate that CD11c(hi) DCs provide a critical and unexpected role to preserve the immune-privileged CNS in lethal neuroinflammation via regulating the differentiation, function, and trafficking of CD11b(+)Ly-6C(hi) monocytes.

19. The generation of mouse line with Flip deficiency in cells that express cre under the CD11c promoter is reported.

20. Probucol effectively retarded atherosclerosis at least partly through lipid-lowering and inhibiting immune maturation of CD11c dendritic cells in STZ-induced diabetic LDLR mice.