anti-Chemokine Binding Protein 2 (CCBP2) Antibodies

Human Chemokine Binding Protein 2 (CCBP2) interaction partners

1. Data suggest that MIRN146b and MIR10b directly bind 3'-untranslated region of ACKR2 and down-regulate expression of ACKR2 in keratinocytes and in lymphatic endothelial cells, respectively. (ACKR2 = atypical chemokine receptor 2)

2. ACKR2 is induced after traumatic brain injuries and has a significant impact on mortality and lesion development acutely following closed head injury.

3. ACKR2 is a molecular regulator play a role in inflammatory changes in patients with psoriasis.

4. Data indicates that D6 is concentrated on trophoblast cell membranes in pre-eclampsia, in line with higher circulating levels of D6-ligand chemokines, but its scavenging activity is affected by trophoblast cytoskeleton disarrangement.

5. ACKR2 mediates chemokine scavenging by primary human trophoblasts.

6. Data show the structural motifs in the atypical chemokine receptor 2 (ACKR2) are responsible for ligand binding, and suggest ACKR2-derived N-terminal peptides as being of potential therapeutic significance.

7. Data show that low decoy receptor D6 expression correlated to more invasive tumors and that tumor location influences D6 expression, which is lower in the more distal parts of the colon.

8. engagement of the ACR D6 by its ligands activates a beta-arrestin1-dependent, G protein-independent signaling pathway that results in the phosphorylation of the actin-binding protein cofilin through the Rac1-PAK1-LIMK1 cascade.

9. co-expression of DARC, D6, and CCX-CKR significantly associated with higher survival in gastric cancer

10. D6, which is upregulated in both inflammatory and tumor contexts, is an essential regulator of inflammatory leukocyte interactions with lymphatic endothelial cells(LECs) and is required for immature/mature DC discrimination by LECs.

11. We here summarize the knowledge available today on D6 structural and signaling properties and its essential role for the control of inflammatory cells traffic and proper development of the adaptive immune response.

12. CCL2 binding to primary adult human astrocytes is CCR2-independent and is likely to be mediated via the D6 decoy.

13. D6 is expressed in AMs from patients with COPD, and its expression correlates with the degree of functional impairment and markers of immune activation.

14. These data demonstrate a novel role for D6 as a regulator of the transition from uninvolved to lesional skin in psoriasis.

15. Chemokine decoy receptor D6 limits CC-chemokine-dependent pathogenic inflammation and is required for adequate cardiac remodeling after myocardial infarction.

16. DARC and D6, the most studied members of this group of molecules, are reviewed.

17. Chemokne D6 expression is higher in biopsies taken from more severe cardiac allograft rejection.

18. D6 protein is found predominantly inside human choriocarcinoma-derived cells with only a small fraction available on the cell surface at any one time, yet it can progressively remove extracellular chemokines, without apparent desensitization.

19. CCR10 is unlikely to be necessary for cutaneous homing of TH cells in the models studied here. CCR10 may instead play a role in the movement of specialized "effector" cutaneous TH cells to and/or within epidermal microenvironments.

20. In lymphatic vessels D6 acts as a nonsignaling decoy receptor and scavenger for inflammatory CC chemokines, by clearing them and preventing excessive diffusion via afferent lymphatics to lymph nodes.

Mouse (Murine) Chemokine Binding Protein 2 (CCBP2) interaction partners

1. ACKR2 is important in limiting renal inflammation and fibrotic remodeling in progressive nephrotoxic glomerulonephritis.

2. ACKR2 (Ccbp2) is a key regulator of myeloid differentiation and function and its targeting unleashes the anti-metastatic activity of neutrophils.

3. ACKR2 is induced after traumatic brain injuries and has a significant impact on mortality and lesion development acutely following closed head injury.

4. study found that the inflammatory chemokine CCL5 is mostly retained (75%) during the resolution of zymosan A peritonitis in mice; CCL5 exerts a novel proresolving role on macrophages when acting in concert with apoptotic PMN-expressed D6.

5. ACKR2 is an important regulator of branching morphogenesis in diverse biological context; this provide the first evidence of a role for chemokines and their receptors in postnatal development processes.

6. Ackr2 expression levels limits development of cutaneous inflammatory responses in psoriasis.

7. ACKR2 deletion reduced renal inflammation in diabetes and the ultimate response was a high degree of protection from diabetic nephropathy.

8. Ackr2 deficiency does not suppress autoreactive T-cell priming and autoimmune pathology, but can enhance T-cell polarization toward Th17 cells.

9. ACKR2 can regulate fetal growth, placental structure, and neonatal mortality in mice.

10. Further examination revealed that proximity of pro-lymphangiogenic macrophages to developing lymphatic vessel surfaces is increased in ACKR2-deficient mice and reduced in CCR2-deficient mice.

11. some cells, including plasmacytoid dendritic cells, can express both CCR2 and ACKR2; that Ly6C(high) monocytes have particularly strong CCL2-scavenging potential in vitro and in vivo; and that CCR2 is a much more effective CCL2 scavenger than ACKR2.

12. Expression of the D6 receptor mediates dendritic cell function and promotes corneal allograft rejection.

13. Our data therefore indicate that D6 is able to play a cell-autonomous role as a migratory rheostat restricting migration of D6-expressing cells such as neutrophils

14. These data demonstrate a novel role for D6 as a regulator of the transition from uninvolved to lesional skin in psoriasis.

15. results indicate a novel mode of action for D6 during the resolution of inflammation that is instrumental to the shaping of resolving macrophage phenotypes and the completion of resolution

16. Chemokine decoy receptor D6 limits CC-chemokine-dependent pathogenic inflammation and is required for adequate cardiac remodeling after myocardial infarction.

17. control of CCR2 ligands by D6 regulates the traffic of Ly6C(high) monocytes and controls their immunosuppressive potential.

18. D6, by suppressing inflammatory chemokine binding to lymphatic surfaces, and thereby preventing inflammatory leukocyte adherence, is a regulator of lymphatic function and a contributor to the integration of innate and adaptive immune responses.

19. identify novel D6(active) B1-cell subsets, including those we term B1d, which lack CD5 and CD11b but exhibit typical B1-cell properties, including spontaneous ex vivo production of IgM, IL-10, and anti-phosphorylcholine antibody

20. Fetal D6 suppresses inflammation in many mouse tissues, and notably, D6-deficient fetuses in D6-deficient female mice show increased susceptibility to inflammation-driven resorption.