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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.
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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.
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Report anti-PF4/H monoclonal antibody with a human Fc fragment, which induces similar cellular activation as heparin-induced thrombocytopenia antibodies.
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PF4 was produced by Ly6G+CD11b+ immature myeloid cells in the early stage premetastatic lungs, and decreased during metastatic progression.
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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.
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These findings support PF4 as a cancer-enhancing endocrine signal that controls discrete aspects of bone marrow hematopoiesis and tumor microenvironment.
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data support that increased levels of circulating CXCL4 may contribute to immune dysregulation through the modulation of dendritic cell differentiation
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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.
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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.
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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.
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The major aim of this review article was to evaluate the role of CXCL4 in hematological malignancies, promotion of HSC quiescence as well as BM niche cells.
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binding of PF4 to perlecan was found to inhibit both FGF2 signaling and platelet activation
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CXCL4 plays an important role in pancreatic inflammation
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Data suggest that serum haptoglobin, fetuin-A, platelet factor-4, hs-CRP (high sensitive-C-reactive protein), SAP (serum amyloid P), AGP (alpha1-acid glycoprotein) levels of adolescents with metabolic syndrome are significantly higher than those of controls subjects.
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The hitherto unknown association of increased serum CXCL4 with features of microvascular impairment in primary Sjogren's syndrome, along with the negative association with features of lymphocytic response suggest clarifying the possible implication of this chemokine in primary Sjogren's syndrome pathogenesis in larger studies.
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serum concentration of CXCL4 was significantly increased in patients with Chronic Liver Allograft Dysfunction (CLAD); CXCL4 mRNA was significantly increased in subjects with CLAD versus individuals without CLAD
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Plasma levels of CXCL4 are associated with tumour vascularity.
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Data suggest that, in patients with hypothyroid autoimmune thyroiditis, PF4/CXCL4 serum levels are significantly lower in those with subclinical hypothyroidism than in euthyroid control subjects.
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Expression of CXCL4 and aquaporin 3 and 10 mRNAs in middle ear effusion is associated with the pathophysiology of otitis media with effusion.
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PF4 changed its structure upon binding to polyP in a similar way as seen in PF4/heparin complexes. PF4/polyP complexes exposed neoepitopes to which human anti-PF4/heparin antibodies bound.
