Platelet Factor 4 (PF4) ELISA Kits

Human Platelet Factor 4 (PF4) interaction partners

1. Findings demonstrate a novel T-cell regulatory function of non-platelet-derived CXCL4 that colon cancer cells may hijack to evade the host immune system.

2. CXCL4 inhibits endothelial cell proliferation and migration, leading to suppression of angiogenesis.

3. CXCL4 induced CCR1 endocytosis and could induce monocyte chemotaxis in a CCR1 antagonist-sensitive manner.

4. Cellular immune sensitization to PF4-heparin complexes occurs before heparin exposure, and immune dysregulation can contribute to heparin-induced thrombocytopenia.

5. Platelets are able to kill bacteria directly after recognizing anti-PF4/P IgG opsonized bacteria in the presence of PF4 via their FcgammaRIIA.

6. Observations suggest the crucial role of platelet cytokine PF4 as the rapid enhancer of replication as well as propagation of both observations together suggest the crucial role of platelet cytokine PF4 as the rapid enhancer of replication as well as propagation of both Dengue virus and Japanese Encephalitis virus in host cells including monocytes by inhibiting IFN response of these immune cells.

7. Study elucidate an unanticipated mechanism for CXCL4-mediated immune amplification in systemic sclerosis, in which CXCL4 organizes "self" and microbial DNA into liquid crystalline immune complexes that amplify TLR9-mediated plasmacytoid dendritic cell hyperactivation and interferon-alpha production. Surprisingly, this activity does not require CXCR3, the CXCL4 receptor.

8. Urinary angiostatin, CXC chemokine ligand 4 (CXCL4) and vascular cell adhesion molecule-1 (VCAM-1) were significantly higher in patients with active renal disease than in patients with active non-renal disease.

9. results identify PF4 as a ligand for the integrin Mac-1 and suggest that many immune-modulating effects previously ascribed to PF4 are mediated through its interaction with Mac-1

10. Bacteremia/sepsis was associated with higher anti-PF4/heparin antibody titers. There was no difference between Gram negative/positive bacteremia and antibody titer.

11. CXCL4 boosts pro-inflammatory cytokine production especially IL-17 by CD4(+) T cells, either by acting directly or indirectly via myeloid antigen presenting cells, implicating a role for CXCL4 in psoriatic arthritis pathology.

12. The data show that antibodies magnify immune responses induced in PBMCs by PF4 alone or in complex with heparin or LMWH. Authors propose that following induction of HIT antibodies by heparin-PF4 complexes, binding of the antibodies to PF4 is sufficient to induce a local pro-inflammatory response which may play a role in the progression of HIT.

13. Report anti-PF4/H monoclonal antibody with a human Fc fragment, which induces similar cellular activation as heparin-induced thrombocytopenia antibodies.

14. PF4 was produced by Ly6G+CD11b+ immature myeloid cells in the early stage premetastatic lungs, and decreased during metastatic progression.

15. The CXCL4 monomer acts as the minimal active unit for interacting with CXCR3 N-Terminal Sulfated Peptide, and sulfation of N-terminal tyrosine residues on the receptor is important for binding.

16. These findings support PF4 as a cancer-enhancing endocrine signal that controls discrete aspects of bone marrow hematopoiesis and tumor microenvironment.

17. data support that increased levels of circulating CXCL4 may contribute to immune dysregulation through the modulation of dendritic cell differentiation

18. Endometrial CXCL4 mRNA concentrations were significantly increased during menstruation. In women with heavy menstrual bleeding, CXCL4 was reduced in endothelial cells during the menstrual phase compared with women with normal menstrual bleeding. These data implicate CXCL4 in endometrial repair after menses.

19. Two haplotype blocks, one upstream to the coding region of UGT2A1 (rs146712414, P = 9.1 x 10(-5); odds ratio [OR], 1.34; 95% confidence interval [CI], 1.16-1.56) and one downstream of the genes PF4/PPBP/CXCL5 (rs1595009, P = 1.3 x 10(-4); OR, 1.32; 95% CI, 1.15-1.52), were associated with AgP.

20. These data demonstrate that the CXCR2 network and CXCL4 play a role in the maintenance of normal HSC/HPC cell fates, including survival and self-renewal.

Mouse (Murine) Platelet Factor 4 (PF4) interaction partners

1. ELF4 binds to the promoter of genes of two C-X-C chemokines, Pf4 and pro-platelet basic protein (Ppbp), initiating the transcription of these two genes, thereby enhancing PF4-mediated killing of parasites from infected erythrocytes.

2. Platelets are activated during P. aeruginosa infection, and mice depleted of platelets display markedly increased mortality and impaired bacterial clearance. CXCL4 deficiency impairs bacterial clearance and lung epithelial permeability. CXCL4 deficiency selectively regulates chemokine production. CXCL4 deficiency reduces platelet-neutrophil interactions in blood following P. aeruginosa infection.

3. these data demonstrate that PF4 has an important role in increasing B cell differentiation in the bone marrow environment

4. these results identify CXCL4 as a vital immunoregulatory chemokine essential for protecting mice against influenza A virus infection, especially as it affects the development of lung injury and neutrophil mobilization to the inflamed lung

5. These results indicate that CXCL4 is a novel Ni-binding protein that augments Ni allergy at the elicitation and sensitization phases. This is the first study to demonstrate that the Ni-binding protein augments Ni allergy in vivo.

6. PF4 was produced by Ly6G+CD11b+ immature myeloid cells in the early stage premetastatic lungs, and decreased during metastatic progression.

7. These data demonstrate that the CXCR2 network and CXCL4 play a role in the maintenance of normal HSC/HPC cell fates, including survival and self-renewal.

8. Platelet-derived CXCL7 and CXCL4 contribute to the pathogenesis of acute lung injury.

9. CXCL4 plays an important role in pancreatic inflammation

10. Platelet secretion of CXCL4 is Rac1-dependent and regulates neutrophil infiltration and tissue damage in septic lung damage

11. PF4 has a complex intramedullary life cycle with important implications in megakaryopoiesis and hematopoietic stem cell replication not seen with other tested alpha granule proteins.

12. Heparin enhances antigen uptake and activation of the initial steps in the cellular immune response to PF4-containing complexes.

13. Data indicate that platelet factor 4 (PF4) is involved directly in liver innate immune response against ischaemia-reperfusion injury (IRI) by regulating Th17 cell differentiation.

14. CXCL4 regulates hematopoietic stem cell cell cycle activity.

15. Platelet factor 4 has a role in regulating Th17 differentiation and cardiac allograft rejection

16. Histones regulate activated protein C formation in a manner similar to PF4 and suggest heparinoids may be benificial in sepsis.

17. PF4 drives a vascular smooth muscle inflammatory phenotype including a decline in differentiation markers, increased cytokine production, and cell proliferation.

18. Peptide inhibition of CXCL4-CCL5 interactions may represent a viable translational strategy to limit progression of abdominal aortic aneurysms.

19. PF4 expression on intestinal epithelial cells is increased after IR at both the mRNA and protein levels. In conclusion, these findings demonstrate that may PF4 represent an important mediator of local and remote tissue damage.

20. These results suggest that Cxcl4 and Cxcl7 play a role in the development of neurobehavioral alterations that are triggered by in utero TCDD exposure and later surface in adults.