Leukemia Research, Vol. 3, No. 5, pp. 305-313. 0145-2126/79/1001--0305 $02.00/0 Pergamon Pros, Ltd., 1979. Printed in Great Britain. LYMPHOID ANTIGENS (LY) ON LEUKAEMIC CELL POPULATIONS: RECOGNITION BY MEANS OF ANTILYMPHOCYTIC GLOBULINS AND CLINICAL IMPLICATIONS ALBERTO M. MARMONT, GINO SANTINI, GIOVANNAPIAGGIO, MARIA R. RAFFO, EUGENIO DAMASIO, MICHELE CARELLA, EDOARDOROSSI, DOMENICOGIORDANo, RAFFAELLACERRI, MARIA T. VAN LINT, RENATOVIMERCATI, MARCO RISSO, MARINA PODESTA and ANDREA BACIGALUPO Department of Haematology, Ospedale San Martino, Genova, Italy (Received 24 November 1978. Revised 22 March 1979. Accepted 7 May 1979) Abstract--Cells obtained from 120 cases of acute and chronic leukaemias (both non-lymphocytic, ANL, and lymphoid leukaemias, ALL) were reacted in an indirect immunofluorescencetest with antilymphocytic globulins (ALG) directed against different lymphoid cell populations (spleen, lymph node, tonsil, thymus, thoracic duct, peripheral blood lymphocytes, chronic lymphatic leukaemias cells and cultured lymphoblasts). The aim of this study was to recognize lymphoid antigens expressed on both thymus and bone marrow derived lymphoeytes, as well as on leukaemic cells. Our 4 years' experience cart be summarized as follows: (1) unabsorbed ALGs strongly react with B, T cells, as well as with all leukaemic cells tested; (2) myeloid cross-reactivity can be over- come after proper absorptions with cells from AML or AMoL or CML or with neutrophils from healthy donors; (4) MY-absorbed ALG can still interact with B, T lymphocytes, eLL-cells, blasts from B, T, null ALL and cells from CML in lymphoid blastic crisis, but not with myeloid or monocytic cells; (5) four out of five undifferentiated leukaemias proved to be reactive to ALG, as well as four out of 31 AML. All ALG-positive cases (LY + eases), irrespective of their cytochemical diagnosis, were treated with vincristine--prednisone, with good response rates. The biological and clinical significance of these results are discussed. INTRODUCTION DIFFERENT antigenic determinants can be recognized at the surface of human cells by the use of heteroantisera. Some laboratories have raised antisera directed against "'tumour- associated" or "leukaemia-associated" antigens [6, 12, 13, 16] employing leukaemic cells as immunogens and their normal counterpart for the absorption of antibodies reacting with "physiological" determinants. ALL-associated antigens have been reported to be expressed at the surface of ALL, CML-lyBC and AUL [9, 12, 13] also in the absence of other known markers such as surface immunoglobulins (Slgs) or T cell antigens. Other investigators have employed viral antigens to produce specific antisera and have reported one particular viral antigen to be expressed at the surface of cells from CML [21]. The precise genetic origin of these antigens is uncertain although there is evidence to suggest that some are in fact normal differentiation antigens of haemopoietic precursors [24]. By contrast, other antisera unequivocally react with determinants expressed on both Abbreviations: ALG, Anti-human lymphocytic globulin; RAH1F, Rabbit anti-horse immunoglobulins; F1TC, Conjugated antisera; ANL, Acute non-lymphocytic leukaemia; AML, Acute myeloid leukaemia; A3IML, Acute myelomonocytic leukaemia; AMoL, Acute monocytic leukaemia; APL, Acute promyelocytic leukaemia; A UL, Acute undifferentiated leukaemia; SCL, Stem cell leukaemia; ALL, Acute lymphoblastic leukaemia; c-ALL, Common ALL; CLL, Chronic lymphocytic leukaemia; CML, Chronic myelogenous leukaemia; CML-lyBC, CML in lymphoid blastic crisis; CML-myBC, CML in myeloid BC; U-AML, Undifferentiated AML; VCR-PRED, vincristine-prednisone treatment. Surface markers: L Y, Lymphoid antigens; ALL, ALL-associated antigens; la, B lymphocyte antigens. 305