Common acute lymphoblastic leukemia antigen CD10

Originally identified on the surface of acute lympho-blastoid leukemia (ALL) cells and designated as common acute lymphoblastoid leukemia antigen (CALLA), the antigen has now been assigned the cluster of differentiation number 10 (CD 10). CALLA was initially recognized using rabbit antiserum raised against ALL cells which had been precoated with rabbit antibodies against antigenic determinants present on normal lymphocytes. The rabbit anti-CALLA sera were found to produce a maximal reactivity against peripheral blood nucleated cells from ALL patients, and a minimal reactivity when tested against normal bone marrow cells or cells from patients with leukemias other than ALL. Using monoclonal antibodies, the distribution of CALLA cells has been further clarified. Thus very few CALLA' cells are present in peripheral blood samples from normal individuals, while CALLA cells, coexpressing immunoglobulin M (IgM) molecules and CD19, are detectable in fetal bone marrow and peripheral blood samples. CALLA fetal bone marrow cells, cultured with interleukin 2 (IL-2) and irradiated feeder thymocytes can differentiate to CD2 1, CD3 ' cells expressing either CD4 or CDS. These findings are consistent with early data suggesting that CALLA molecules are expressed on B and T cells during early stages of fetal development. CALLA+ cells are detectable in a majority of patients with B-ALL, in a proportion of T-ALL patients and in some cell lines derived from T cell non-Hodgkin lymphoma (T-NHL). The antigen is expressed in about one-third of Ph1 chromosome-positive leukemia patients during blast crisis.

The molecular nature of CD10 has now been partially defined; cDNA clones have been isolated, sequenced and shown to control the synthesis of a protein structurally identical to the human membrane-associated enzyme neutral endopeptidase (NEP

The biological enzymatic role of CD 10 molecules has not yet been clarified, but it has been suggested that CD10-NEP mediates chemotaxis and that the presence or absence of CD10-NEP might affect the clinical course of ALL in childhood. It seems, in fact, that CD 10" patients with ALL have shorter disease-free survival.

Elucidation of the biological function of CD10 molecules expressed on subpopulations of lymphocytes during fetal life and in patients with leukemia might only be obtained once the specific substrate of this enzyme has been identified.

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