Papers by Ellinor Peerschke
Molecular Immunology, 2004
A growing body of evidence supports the hypothesis that atherosclerosis has an inflammatory compo... more A growing body of evidence supports the hypothesis that atherosclerosis has an inflammatory component, and that immune mechanisms, including complement activation, are likely to be involved. gC1q-R/p33 (gC1q-R) is a multifunctional and multicompartmental cellular protein, which is postulated to play a role in inflammation and thrombosis by interacting with C1q and high molecular weight kininogen (HK). To examine the expression of gC1q-R and its major ligands, C1q and HK, in human atherosclerotic lesions, sections of carotid arteries removed during endarterectomy and coronary arteries obtained at autopsy were stained with specific polyclonal or monoclonal antibodies. Control sections were stained with irrelevant rabbit IgG or isotype matched murine monoclonal antibody (MOPC), respectively. Tissue sections were counterstained with hematoxylin and examined by light microscopy. Specific staining for gC1q-R, C1q, and HK was observed in and around atherosclerotic lesions. In contrast to control antibodies, antibodies directed against gC1q-R reacted with endothelial cells, foam cells, smooth muscle cells, and inflammatory cells present in the intima and media of atherosclerotic lesions. In addition, the necrotic central core of advanced lesions with calcifications, fibrin, and lipids, stained intensely for gC1q-R, and negligibly with control antibodies. HK demonstrated a similar staining pattern, whereas C1q was most heavily expressed in the fibrous cap and necrotic core of atherosclerotic lesions. The localization of gC1q-R and its ligands C1q and HK in atherosclerotic lesions, and the previously described ability of gC1q-R to modulate complement, kinin, and coagulation cascades, suggest that gC1q-R may play an important role in promoting inflammation and thrombosis in atherosclerotic lesions.
Bookmarks Related papers MentionsView impact
Proceedings of the …
Bookmarks Related papers MentionsView impact
International Journal of Cancer Research and Molecular Mechanisms ( ISSN 2381-3318 ), 2015
Bookmarks Related papers MentionsView impact
Transfusion, Jan 21, 2015
Successful peripheral blood stem cell transplantation (PBSCT) depends on the collection and infus... more Successful peripheral blood stem cell transplantation (PBSCT) depends on the collection and infusion of adequate numbers of peripheral blood progenitor cells (PBPCs). Several predictors of PBPC yield are used currently, including white blood cell (WBC) count and CD34 analysis. This study evaluated the utility of the new automated hematopoietic progenitor cell count available on Sysmex XN hematology analyzers (XN-HPCs) in PBSCT. The performance characteristics of XN-HPC, CD34+, and WBC analysis were compared using 107 matched peripheral blood and apheresis samples. Good correlation was observed between XN-HPC and CD34+ cell counts in peripheral blood (r = 0.88; slope, 0.81) and apheresis collections (r = 0.91; slope, 0.89). Moreover, peripheral blood XN-HPC and CD34 analysis showed comparable ability to predict successful PBPC harvests (≥2 × 10(6) CD34+ cells/kg). At a cutoff of 20 × 10(6) progenitor cells/L, peripheral blood XN- HPC and CD34 analysis both showed negative predictive ...
Bookmarks Related papers MentionsView impact
American journal of clinical pathology, 2014
Evaluation of anemia, particularly iron deficiency, in patients with cancer is difficult. This st... more Evaluation of anemia, particularly iron deficiency, in patients with cancer is difficult. This study examined using the hemoglobin content of reticulocytes (RET-He) to rule out iron deficiency, as defined by serum iron studies (transferrin saturation <20%, serum iron <40 μg/dL, and ferritin <100 ng/mL), in an unselected cancer patient population. Patients were entered into the study based on the existence of concurrent laboratory test requests for CBC and serum iron studies. Using a threshold of 32 pg/cell, RET-He ruled out iron deficiency with a negative predictive value (NPV) of 98.5% and 100%, respectively, in the study population (n = 209) and in a subpopulation of patients with low reticulocyte counts (n = 19). In comparison, the NPV of traditional CBC parameters (hemoglobin, <11 g/dL; mean corpuscular volume, <80 fL) was only 88.5%. These results support the use of RET-He in the evaluation of iron deficiency in a cancer care setting.
Bookmarks Related papers MentionsView impact
Molecular Immunology, 2008
"Complement protein C1q plays a crucial role in regulating peripheral tolerance by facilitat... more "Complement protein C1q plays a crucial role in regulating peripheral tolerance by facilitating clearance of apoptotic debris and modulating T cell proliferation. Moreover, C1q is emerging as a moderator of dendritic cell (DC) activity. Immature DCs (iDC) secrete C1q; we therefore postulated that such endogenously secreted C1q may regulate the transition from monocytes to DCs. Using human peripheral blood monocytes as DC precursors, we show here that monocyte-derived DC growth in the presence of soluble C1q resulted in the failure to down-regulate CD14 and in the reduced expression of DC maturation markers (CD83 and CD86). The inhibition of DC maturation was not due to apoptosis, as assessed by lack of annexin V binding and morphological examination. Instead, multiparametric flow cytometric analysis revealed the development of CD14hiCD11chiCD16+/− cells representing a subset of iDCs. Monocyte–DC precursors from the outset expressed gC1qR, the receptor for globular heads of C1q. In contrast, cC1qR (calreticulin), the receptor for the collagen tails of C1q, was lacking on these cells despite the expression of its putative partner CD91, indicating that inhibition of DC growth by C1q may occur via C1q–gC1qR interactions. Our data therefore suggest that C1q operates at a critical checkpoint during the monocyte to DC transition and helps maintain immune tolerance by signalling possibly via gC1qR. More importantly, our data supports the postulate that pathogens capable of mimicking C1q, such as hepatitis C virus, bind to gC1qR on monocyte–DC precursors to prevent immunogenic DC activity and thus escape the acquired immune response. Supported by NIH Grant R01 AI-060866 (to BG) and R03 AR-05396 (to FSS). "
Bookmarks Related papers MentionsView impact
Frontiers in immunology, 2014
The ability of circulating blood monocytes to express C1q receptors (cC1qR and gC1qR) as well as ... more The ability of circulating blood monocytes to express C1q receptors (cC1qR and gC1qR) as well as to synthesize and secrete the classical pathway proteins C1q, C1r, and C1s and their regulator, C1-INH is very well established. What is intriguing, however, is that, in addition to secretion of the individual C1 proteins monocytes are also able to display macromolecular C1 on their surface in a manner that is stable and functional. The cell surface C1 complex is presumably formed by a Ca(2+)-dependent association of the C1r2⋅C1s2 tetramer to C1q, which in turn is anchored via a membrane-binding domain located in the N-terminus of its A-chain as shown previously. Monocytes, which circulate in the blood for 1-3 days before they move into tissues throughout the body, not only serve as precursors of macrophages and dendritic cells (DCs), but also fulfill three main functions in the immune system: phagocytosis, antigen presentation, and cytokine production. Since the globular heads of C1q wi...
Bookmarks Related papers MentionsView impact
Blood, 1983
A murine monoclonal antibody directed at or near a platelet membrane receptor for the von Willebr... more A murine monoclonal antibody directed at or near a platelet membrane receptor for the von Willebrand factor was produced by the hybridoma technique. Purified F(ab')2 fragments and/or intact antibody completely blocked the agglutination of platelets induced by both ristocetin and bovine von Willebrand factor and the binding of von Willebrand factor antigen to platelets. The antibody also decreased platelet retention, prevented the reduction in platelet electrophoretic mobility caused by bovine von Willebrand factor, and decreased the serum prothrombin time. Radiolabeled F(ab')2 fragments bound to or approximately 2.5 X 10(4) sites on normal platelets with high affinity (KD or approximately 1.5 X 10(-8) M); there was no binding to platelets from 2 patients with the Bernard-Soulier syndrome. Immunoprecipitation and affinity chromatography studies indicated that the antibody binds to glycoprotein lb at a site contained on the externally oriented portion of the GPIb alpha chain (...
Bookmarks Related papers MentionsView impact
Advances in Experimental Medicine and Biology, 2008
Bookmarks Related papers MentionsView impact
Journal of the American College of Cardiology, 2011
Bookmarks Related papers MentionsView impact
Journal of Clinical Investigation, 1983
Bookmarks Related papers MentionsView impact
Journal of Allergy and Clinical Immunology, 2009
Bookmarks Related papers MentionsView impact
International Journal of Stroke, 2008
Bookmarks Related papers MentionsView impact
Clinical Chemistry, 2006
Bookmarks Related papers MentionsView impact
Annals of the New York Academy of Sciences, 1983
Bookmarks Related papers MentionsView impact
…, 1980
Page 1. 1980 55: 841-847 EI Peerschke, MB Zucker, RA Grant, JJ Egan and MM Johnson aggregability ... more Page 1. 1980 55: 841-847 EI Peerschke, MB Zucker, RA Grant, JJ Egan and MM Johnson aggregability Correlation between fibrinogen binding to human platelets and platelet http://bloodjournal.hematologylibrary.org/misc/rights ...
Bookmarks Related papers MentionsView impact
American Journal of Clinical Pathology, 2007
Bookmarks Related papers MentionsView impact
American Journal of Clinical Pathology, 2009
Bookmarks Related papers MentionsView impact
Journal of Histochemistry & Cytochemistry, 2012
Bookmarks Related papers MentionsView impact
Uploads
Papers by Ellinor Peerschke