Host defense deficiency in hairy cell leukemia and its correction by leukocyte transfusion

E. M. Hersh, S. Murphy, A. Zander, K. Dicke, D. J. Stewart, H. Toki, J. Latreille

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

A similar defect in host defense mechanisms in hairy cell leukemia was defined in two patients. Surface-adherent monocytes were not detected in the peripheral blood nor were monocytes that mediate antibody-dependent cell-mediated cytotoxicity (ADCC) to isoantibody-coated human erythrocytes. In addition, lymphocytes of both patients failed to show blastogenic responses to concanavalin A (Con-A) and pokeweed mitogen (PWM) but showed a vigorous response to phytohemagglutinin (PHA). Other immunologic abnormalities were present but were either moderate in degree or were not present in both patients. In vitro lymphocyte blastogenic responses were fully restored by incubation of patients' leukocytes with a normal donor's adherent monocytes. One patient received daily allogenic leukocyte transfusions for 4 days. This resulted in complete normalization of monocyte adherence and ADCC that persisted for several months after transfusion and was associated with hematologic improvement. Therapy in case 1 resulted in correction of the blastogenic transfusion and was associated with hematologic improvement. Therapy in case 1 resulted in correction of the blastogenic responses to Con-A and PWM. Thus, a host defense defect in hairy cell leukemia has been defined in 2 patients and a preliminary result suggests that therapy with leukocyte transfusions may be useful in the postsplenectomy patient with an infectious complication and should be explored further.

Original languageEnglish (US)
Pages (from-to)526-533
Number of pages8
JournalUnknown Journal
Volume56
Issue number3
DOIs
StatePublished - 1980
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

Fingerprint

Dive into the research topics of 'Host defense deficiency in hairy cell leukemia and its correction by leukocyte transfusion'. Together they form a unique fingerprint.

Cite this