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©Ferrata Storti Foundation review Haematologica 1994; 79:374-386 REPORT ON THE FIFTH INTERNATIONAL WORKSHOP ON HUMAN LEUKOCYTE DIFFERENTIATION ANTIGENS, BOSTON, NOVEMBER 3-7, 1993 Francesco Lanza, Sabrina Moretti, Stefano Papa*, Fabio Malavasi°, Gianluigi Castoldi Institute of Hematology, University of Ferrara; *Dept. of Morphology Sciences, University of Urbino; °Dept. of Genetics, Biology and Medical Chemistry, University of Turin, Italy his paper represents a detailed descrip- and those of undefined specificity (the so-called tion of the results and basic studies pre- blind panel), were submitted to extensive multi- Tsented at the 5th International Workshop disciplinary studies that included flow cytome- on Leukocyte Differentiation Antigen held in try, biochemical, molecular, histochemical and Boston on November 3-7, 1993. More than 500 serologic analysis. Antibody reactivity was eval- institutions worldwide participated in the uated against more than 80 cell types, and, Workshop study groups, and approximately when possible, flow cytometry data have been 1450 antibodies were investigated, allowing the expressed in the form of molecular equivalents identification of 48 new CD clusters and the of soluble fluorochrome (MESF), which should redelineation of 14 previously clustered mole- be considered the reference unit standard for cules (see Table 1). All the monoclonal antibod- the quantitation of fluorescence emission by ies (mAbs) were analyzed by flow cytometry and mAbs at the present time. In order to achieve the data recorded in a Leukocyte Differentiation this goal, it was necessary to use together with Antigen Database (LDAD), which represents the the required mAbs, FITC or PE (as pertinent) source of the information found in this work- pre-mixed quantitative microbead calibration shop report. A more extensive account of this standards, which permitted a comparison Workshop will be published by Oxford between the fluorescence intensity of cells University Press before the end of 1994. stained for the required antibodies and that The workshop was divided into 11 sections expressed by calibration microbeads. The cal- and the workshop organizers were the follow- culation of MESF was based on the evaluation ing scientists: Stuart Schlossman, Chairman of of the peak channel expressed by cells and dif- the Meeting, Laurence Boumsell (T-cell sec- ferent populations of microbeads (four or five, tion), Wally Gilks (Statistical analysis), John depending on the type and source of beads). Harlan (Endothelial cells), Tadamitsu Kishi- The values for the slope, intercept and correla- moto (Cytokine receptors), Chikao Morimoto tion coefficient allowed calculation of the (Activation antigens), Jerome Ritz (NK anti- regression line, which gave precise information gens), Stephen Shaw (Cross-lineage blind on the linearity and stability of the instrument panel), Timothy Springer (Adhesion section), response, the noise level of the flow cytometer, Roy Silverstein (Platelets), Thomas Tedder (B the MESF values of the stained and unstained cells), Robert Todd (Myeloid cells). cells, the resolution indexes for fluorescence, As in previous workshops (Paris: 1982; and the coefficient of variation (CV) of micro- Boston: 1984; Oxford: 1986; Vienna: 1989) all bead fluorescence. The minimum detection mAbs including previously established CD threshold (also termed calculated sensitivity or (CD1-CDw78), candidates for CD designation, instrument fluorescence threshold) of the flow Correspondence: Dr. Francesco Lanza, Institute of Hematology, St. Anna Hospital, via Giovecca 203, 44100 Ferrara, Italy. Tel. international +39.532.295508. Fax. international +39.532.212142. Acknowlegdments: this work was supported by CNR, ACRO project (Ferrara), University of Turin and CNR (Turin). S.M. is the recipient of a grant from AIRC. F.L. is especially indebted to Prof. Stephen Shaw (Experimental Immunology Branch, National Institutes of Health, Bethesda, USA) for giving him to access to the Leukocyte Differentiation Antigen Database (LDAD) software program. Received April 22, 1994; accepted May 24, 1994. 376 5th International Workshop on Leukocyte Differentiation Antigen cytometer corresponds to the MESF value for its human gene location on chromosome 11 at the blank beads, and provides meaningful data band q12-q22. CD98 mAbs inhibit lectin- on the sensitivity of the instrument in detecting induced mitogenesis of human T cells by 50%, fluorescence signals. Using microbeads has the but do not inhibit T-cell-mediated antibody- added advantage of allowing a comparison of dependent cellular cytotoxicity or NK-cell- flow cytometry data over time and between one mediated cytotoxicity; therefore the function of laboratory and another, and of permitting easy this molecule seems to be concerned with cell calculation of the number of binding sites pre- activation and proliferation. CD98 is also comi- sent per cell after staining with the various togenic for T cells incubated with anti-CD3 and mAbs. soluble CD2 mAbs. This molecule enhances The CD system (CD stands for cluster of des- Ca++ flux mediated by Na+/Ca++ exchangers. ignation) for classifying monoclonal antibodies CD98 is weakly expressed on resting T lympho- and their specific antigens was established at cytes, but the antigen levels significantly the first workshop on leukocyte differentiation increase following lectin or alloantigenic T-cell antigens (Paris: 1982), where the rule was also stimulation. Thymocytes, monocytes, endothe- introduced that at least two mAbs that recog- lial cells, stromal cells, epithelial cells, ker- nize the same molecule are required in order to atinocytes, T cell lines and some myeloid cell assign a new CD. It was further recommended lines were found to be reactive with CD98 that the term CD be used for the clustered anti- mAbs. Almost all actively dividing cells strongly bodies and the term CD molecule or CD antigen express this antigen. The eleven mAbs (clones: be used for antigens. 4F2; GRV1; HuLy m10; KS-4; KS-7; L 289; BU The CDw (w stands for workshop) designa- 53, etc.) produced so far have been found to be tion was to be given to those reagents whose specific for the heavy chain. No mAbs are avail- reactivity had not been completely defined, and able for the light chain. therefore would have to be re-evaluated in future workshops. However, a number of mole- CD99. This identifies MIC2 (also termed E2 cules, like glycolipids, cannot be evaluated by or GRP2), which is involved in rosette forma- immunoprecipitation studies, and therefore a tion with sheep or human erythrocytes. Four CD cluster can also be defined in the absence of mAbs (clones: 0662; 12E7; 013; MEM-131) rec- detailed biochemical data or of the molecular ognize this molecule, which has a molecular weight. weight of 32 kD. It is expressed on human T A brief description of the 48 new CD clusters cells, thymocytes, B cells, NK cells, endothelial and the 14 CD groups re-defined during this cells, myeloid cell lines (HL60, etc.) and, to a workshop is presented in the following sections lesser extent, on CD34+ bone marrow progeni- of this report, which is subdivided into 9 head- tor cells. Its gene location is chromosome ings according to the preferential cell-type Yp11.2. binding of mAbs. A brief description of some previously established clusters, which were not CD99R. This molecule functions as CD99 submitted to redefinition during this workshop 32kD restricted. Six mAbs (clones: FMC29; is also given later on, since the novelty of the HI147; HI170; HIT4; D44; L129) identify this results was, in our opinion, noteworthy. antigen, which is expressed on activated T cells, monocytes, endothelial and stromal cells. T section (5 new CD molecules) CD100. This antigen, with a molecular weight CD98. This antigen is a disulfide-linked 125 of 40 kD, is also referred to as BB18 or GR3. kD heterodimeric membrane glycoprotein con- Five mAbs (clones: 148-2D12; A8; BB18; BD16; sisting of 2 chains: an 80-90 kD glycosylated F937G2) have been identified so far that recog- heavy chain and a 40 kD nonglycosylated light nize this molecule. Both PHA-stimulated and chain. This molecule is also called 4F2 and has resting T cells express this antigen; a weak posi- F. Lanza et al. 377 tivity has also been found on B cells, mono- tors) does not bind GM-CSF, but its association cytes, neutrophils, and fetal T lymphocytes. with the Ͱ-subunit generates high affinity receptors for GM-CSF. The human gene loca- CDw101. This molecule has a molecular tion of the Ͱ-subunit is Xp22.32,Yp11.3. Its weight of 140 kD; it is also known as GR14, function is to promote the growth and differen- BA27 or BB27. The two mAbs (clones: BA27; tiation of neutrophils, eosinophils and mono- BB27) belonging to this cluster react with a cytes from bone marrow multipotent precur- subset of PHA-stimulated and resting T cells, sors. GM-CSF induces tyrosine phosphoryla- NK cells, monocytes and endothelial cells. tion of a set of proteins similar to IL-3; engage- ment of the receptor also results in activation of tyrosine kinases, GTP binding proteins (G-pro- NK section (1 new CD molecule) teins), and increased expression of CD35 (com- CD57. This 110 kD molecule is present on plement receptor 1) and CD11/CD18 antigens. large granular lymphocytes, a subset of CD8+ It also induces glucose transport, ion fluxes and cells, and a small subset of CD4+/CD45RO+ T the expression of a variety of genes. The only cells in the germinal center of lymph nodes. It is mAb (clone: hGMCSFR-M1) that has been also found on a substantial subset of CD4+ cells defined as recognizing this molecule reacts with from renal allograft recipients, and on a monocytes, neutrophilic granulocytes, myeloid CD4+/CD7– T-cell subpopulation from HIV- and monocyte precursors, CD34+ (middle infected (human immunodeficiency syndrome) intensity) hematopoietic progenitors, B and T patients. Furthermore, in patients with HIV fetal lymphocytes, endothelial cells, fibroblasts, infection the number of CD4+/CD57+ cells HL60, KG1a and U937 cell lines. Breast and increases with the advancing stage of the dis- lung carcinoma cell lines, as well as osteogenic ease, suggesting a role for this marker in the cell lines are stained by CD116 antibodies.
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