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Expression of cytoadhesion molecules (CD56, CD54, CD18 and CD29) by myeloma plasma cells
Author(s) -
Riet Ivan,
Waele Mark De,
Remels Linda,
Lacor Patrick,
Schots Rik,
Camp Benjamin Van
Publication year - 1991
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1991.tb08050.x
Subject(s) - cell adhesion molecule , integrin , plasma cell , immunophenotyping , biology , multiple myeloma , intercellular adhesion molecule , antigen , microbiology and biotechnology , bone marrow , monoclonal antibody , neural cell adhesion molecule , antibody , cell adhesion , pathology , immunology , cell , medicine , biochemistry
Recently we reported the expression of the human natural killer cell associated antigen CD56 (Leu 19/NKH1) in plasma cells of a majority of multiple myeloma (MM) patients. CD56 is known to be an isoform of the human neural adhesion molecule N‐CAM which is involved in homotypic adhesive interactions. By immunophenotyping using four CD56 specific monoclonal antibodies and immunoprecipitation analysis we here confirm that the Leu 19 antigen expressed by myeloma plasma cells is identical to N‐CAM and corresponds to the 145 kDa isoform. Because of the possible biological role of adhesion molecules on myeloma cells, we compared the expression of N‐CAM with the intercellular adhesion molecule 1 (ICAM‐1) and the β1 and β2 integrins. By immunogold‐silver staining of cytospin preparations of mononuclear cell suspensions, bone marrow plasma cells of 17 MM patients were analysed. Plasma cells expressed N‐CAM (CD56) in 14 patients, ICAM‐1 (CD54) in 16 patients, and β2 intergrins (CD18) in eight patients. β1 integrins (CD29) were expressed in all patients. The expression of β2 integrins was always very weak while N‐CAM, ICAM‐1 and the β1 integrins showed a moderate to strong positivity. The plasma cells of five haematological normal individuals lacked significant N‐CAM expression but were positive for ICAM‐1 and both integrin subgroups. One plasma cell leukaemia patient and two out of four end‐stage MM patients showed no expression of N‐CAM or β2 integrins on their circulating plasma cells. Among 11 previously established myeloma cell lines, surface expression of ICAM‐1 and the integrins was detected in most cases, while N‐CAM was present in only four lines. Most cell lines showed coexpression of the fibronectin receptors (VLA‐4 and VLA‐5) and the laminin receptor (VLA‐6). The collagen receptor (VLA‐2) was not expressed. The N‐CAM negative cell lines included four cell lines that were derived from plasma cell leukaemia patients. These results indicate that the expression of adhesion molecules is an intrinsic part of the biology of multiple myeloma.