Transferrin receptors on human reticulocytes: variation in site number in hematologic disorders.

Assays of binding of 125iodine-labeled (125I) human transferrin were used to study transferrin receptor sites on reticulocytes from 15 normal subjects and from 66 patients with various hematologic disorders. In normal subjects, few or no transferrin receptors were detected whereas the average number of receptors per reticulocyte varied greatly from patient to patient, ranging from 0 to 67,700 in samples, from 35 patients, on which Scatchard analysis of binding of [125I]-transferrin was done. Marked heterogeneity in the number of reticulocyte transferrin receptors in different hematologic disorders was also found in assays with [125I]-OKT9 (monoclonal antibody to the human transferrin receptor). The number of receptors was not correlated with either the reticulocyte count or the hemoglobin.

An antigen shared by human granulocytes, monocytes, marrow granulocyte precursors and leukemic blasts.

An antibody to human granulocytes was raised in rabbits by immunization with granulocytes pretreated with rabbit antibody to contaminating antigens. The antibody reacted not only with granulocytes but also with monocytes and bone marrow granulocyte precursors including colony-forming units in culture (CFU-C). In tests with leukemic cells, the antibody reacted with blasts from most (8 of 9) patients with acute myelomonoblastic leukemia and from some patients with acute myeloblastic leukemia, morphologically undifferentiated acute leukemia and chronic myelogenous leukemia in blast crisis. The antibody did not react with blasts from patients with acute lymphoblastic leukemia nor with leukemic cells from patients with chronic lymphocytic leukemia.

Diagnosis of haematological disease using anti-i. II. Distinction between acute myeloblastic and acute lymphoblastic leukaemia.

Leukaemic blast cells were obtained from the blood of six patients with acute lymphoblastic leukaemia (ALL) and 15 patients with acute myeloblastic leukaemia (AML). The blasts were compared with lymphocytes from normal subjects in cytotoxicity and 125I-labelled antibody binding tests using several examples of anti-i. As much i antigen was detected on ALL blasts as on normal lymphocytes; much less i antigen was detected on AML blasts. Studies of three patients with morphologically undifferentiated acute leukaemia suggest that, in tests with anti-i, blasts from such patients react either like lymphoblasts or myeloblasts despite the absence of the corresponding morphological features.

Diagnosis of haematological disease using anti-i. I. Disorders with lymphocytosis.

Using cytotoxicity and antibody-binding tests, the i antigen was measured on the blood lymphocytes of normal subjects and of patients in whom a diagnosis of chronic lymphocytic leukemia (CLL) was considered because of a slight lymphocytosis in the blood and bone marrow. Among 25 patients, 15 had a normal amount of i antigen; in 10 there was a marked reduction in i antigen, such as is found in typical CLL. Similar studies were done on lymphocytes from 15 patients with clinical and morphological findings usually associated with lymphosarcoma cell leukemia (LSL). Nine had a normal amount of i antigen; in six there was a marked reduction of i antigen, suggesting a diagnosis of CLL. A study of the subsequent clinical course and final diagnosis in these patients suggests that the reduction in lymphocyte i antigen characteristic of typical CLL occurs in patients with early CLL who have only slight lymphocytosis, but not in patients with slight lymphocytosis from other causes. Similarly, a reduction in lymphocyte i antigen is found in patients with morphologically atypical CLL but not in patients with LSL.

Evidence that blood group A antigen on lymphocytes is derived from the plasma.

Serum from group O volunteers, who had been injected with porcine A blood group substance, was used in lymphocytotoxicity tests. Positive reactions were obtained only with lymphocytes of group A secretors; the strongest reactors were Le(a--b--). The same group O sera reacted with group O lymphocytes which had been exposed to a glycosphingolipid fraction prepared from the plasma of A,Le(a--b--) secretors. These reactions were specifically inhibited by A substance. It is suggested that, unlike the A antigen on red cells, the A antigen detected in lymphocytotoxicity tests is entirely derived from the plasma.