A rapid, single step technique for determination of B and T cell surface markers in malignant lymphoid cells.

The immunological classification of lymphocytic subpopulations has become increasingly important in the treatment of hematologic malignancy. In the present study, the standard techniques for the identification of subsets of both normal and malignant lymphocytes were compared to a new one step procedure for the simultaneous assessment and identification of cells with T or B cell surface markers. With this new technique, cells with T lymphocyte markers form SRBC rosettes and cells with B lymphocyte markers form bead rosettes after incubation with microspheres coated with an anti-immunoglobulin antibody.

ADCC against human erythrocyte target cells: role of the anti-target cell antibodies in determining lymphocyte killer activity.

Studies were undertaken to investigate the role of anti-target cell antibodies in determining whether lymphocytes can mediate antibody-dependent cellular cytotoxicity (ADCC) in vitro. Trinitrophenyl (TNP) modified Chang liver cells and human erythrocytes were employed as target cells and were coated with xenogeneic and allogeneic antibodies against TNP and natural cell surface antigens. Two cytotoxic effector cell populations were used: human peripheral blood mononuclear cells (PBMC) containing both lymphocytes and monocytes, and monocyte-depleted peripheral blood lymphocytes (PBL).

Correlation of adenosine deaminase activity with cell surface markers in acute lymphoblastic leukemia.

Adenosine deaminase (ADA) activity has been measured in the lymphoblasts of 23 untreated patients with acute lymphoblastic leukemia and related to the presence or absence of immunologic cell surface markers. The mean ADA activity in the acute lymphoblastic leukemia population as a whole was increased fourfold over that in normal lymphocytes. 9 of the 23 patients were classified as thymus-derived (T-) cell acute lymphoblastic leukemia on the basis of erythrocyte rosette positivity; the remaining 14 patients had null-cell leukemia.

Immunodeficiency in familial erythrophagocytic lymphohistiocytosis.

4 children with familial erythrophagocytic lymphohistiocytosis and hyperlipidaemia were found to have a previously unrecognised immunological deficiency syndrome which included defects in both humoral and cellular immunity and a plasma inhibitor of in-vitro lymphocyte blastogenesis. The inhibitory activity was proportional to the increase in the triglyceride concentration in the patients' plasma. Immunological deficiency, to which hyperlipidaemia may be a contributing factor, appears to be a significant feature of familial erythrophagocytic lymphohistiocytosis.