Further Characterization of Surface Membrane Structures Expressed on Human Basophils and Mast Cells

Abstract

Recently, we were able to establish the immunologic surface marker profile of human basophils and mast cells. In the present study, the characterization of these cell types was extended by the use of monoclonal antibodies (mAbs) to hemopoietic differentiation antigens. Basophils and mast cells were enriched by mAbs and complement from chronic myeloid leukemia blood (n = 5) and dispersed lung tissue (n = 4), respectively. A panel of 80 mAbs was tested for being reactive with purified cell populations using flow cytometry and/or a combined toluidine blue-immunofluorescence staining procedure. In addition to previous findings, basophils were found to react with mAbs directed against the 126-kilodalton dipeptidylpeptidase IV (CD26), platelet glycoprotein IIa (CD31), CD40 antigen known to share sequence homology with nerve growth factor receptor, leukosialin (CD43), CD44 antigen, the ICAM-1 antigen (CD54) and VIM2-reactive gangliosides involving the sialofucooligosaccharide sequence (CDw65L). Bsp-1 was found to be a specific marker for human basophils, whereas mast cells were not stained by this reagent. Basophils apparently lack CD22 antigen, gangliosides detected by CDw65 mAbs (except CDw65L) and CD71 antigen (transferrin receptor). Mast cells were found to express CD43 and CD44 antigen. In contrast, mast cells lack CD22, CD26, CD31, CD40 and CDw65 antigen. These results provide further evidence that both blood basophils and mast cells express a unique immunologic surface marker profile including binding sites for a variety of immunomodulating ligands and adhesion molecules.

Purification of Normal Human Bone-Marrow-Derived Basophils

“…The phenotype analysis was performed on a FACScan analyser (Becton-Dickinson). The results ob tained are described in table 2 and are in accordance with those published by Valent et al [23] concerning the sur face membrane stuctures expressed on human circulating basophils, except for the presence of HLA-DR. HLA-DR was present on about 45% of our purified basophils and, since this phenotype analysis was performed on 4 samples originating from different cultured bone marrow precur sor cells, this discrepancy may reflect different states of Fig. 2.…”

Signal Transduction by IgG Receptors Induces Calcium Mobilization, but not Histamine Release, in the Human Basophilic Cell Line KU812F

“…Expression of the IgG receptor on basophils was demonstrated using radio-labeled agglgG by Ishizaka et al [33] for the first time. Later, this IgG receptor on basophils was shown to be FcyRlI/CDw32 [10][11][12][13]. Here, we show that stimulation by anti-FcyRll mAb does not provoke histamine release from human basophils.…”

“…On contact with allergen, recruited baso phils are activated through a cross-linking of surface bound IgE molecules and high-affinity IgE receptors, FceRI, lead ing to biochemical signaling events and chemical mediator release [6][7][8][9], Besides FceRI, human basophils also express a number of surface molecules and receptors including Fc receptors K Ä R G E R ' 1996 S. Karger AG. Basel l \ W I \ V J C I \ 1018 2438/96/1091 -0027 $8.00/0 H-Mail karger«/ kargcr.ch Fax +41 61 306 12 34 forlgG [10][11][12][13], Based on the reactivity o f monoclonal anti bodies (rnAbs) and molecular cloning, three different IgG receptors, namely FcyRI (CD64), FcyRll (CDw32) and FcyRIll (CD16) have been identified to date [6.14.15]. Each of them has distinct isoforms that show cell-type-specific expression.…”

“…It has already been shown that human basophils selec tively express FcyRll among IgG receptors [10][11][12][13] al though which isoform of FcyRll is expressed remains to be clarified. In other cell systems, FcyRIIA is known to induce various biological reactions such as phagocytosis or release ofproinflammatory mediators [6,14,15].…”

CD40 expression by human peripheral blood eosinophils.

“…CD40 is a member of the nerve growth factor/TNF receptor superfamily (9)(10)(11). CD40 signaling can be initiated by cross-linking CD40 with anti-CD40 mAb or by interaction with CD40 ligand (CD40L), now referred to as gp39, which is expressed by CD4 ϩ T cells (12)(13)(14) and, as recently shown, by human mast cells and basophils (15,16). The importance of CD40-CD40L interactions in vivo has been recently demonstrated in autoimmune diseases such as collagen-induced arthritis (17), acute and chronic graft-versushost disease (18), and lupus nephritis (19) where treatment of experimental animals with anti-gp39 antibodies markedly prevented disease expression.…”