Effects of interferon-alpha therapy on lymphocyte subpopulations in patients with chronic myeloid leukemia

Stefane Sacchi, Jörge Cortes, Hagop Kantarjian, Moshe Talpaz

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


The mechanism of action of interferon-alpha (IFN-A) in chronic myelogenous leukemia (CML) is not known, but some evidence points at the immune modulation properties of IFN-A. We conducted a prospective analysis on 49 patients with CML in chronic phase treated with IFN-A in order to identify the effect of therapy on different lymphocyte subpopulations as determined by flow cytometric quantification and whether this effect is associated with the response to IFN-A. The absolute number of lymphocytes was similar in all patients regardless of response to IFN-A. In patients achieving a complete cytogenetic response (CCGR) there was a rebound of the absolute count of CD3+, CD4+, CD8+, and CD19+ lymphocytes after discontinuation of therapy with IFN-A. Patients with resistant disease, as well as patients with hematologic response but no cytogenetic response, showed a lower absolute number of CD19+ cells than patients with any cytogenetic response. Patients who achieved a CCGR had a higher absolute number of CD56+ cells than patients with lesser response or no response to IFN-A, and this persisted after discontinuation of therapy. We conclude that an increase in absolute number of CD19+ and CD56+ lymphocytes is observed in CML patients achieving a CCGR with IFN-A compared to patients with lesser responses. These changes could have functional consequences in the control of the disease.

Original languageEnglish (US)
Pages (from-to)41-47
Number of pages7
JournalHematopathology and Molecular Hematology
Issue number1
StatePublished - 1997
Externally publishedYes


  • Chronic myelogenous leukemia
  • Interferon-alpha
  • Lymphocytes

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Hematology


Dive into the research topics of 'Effects of interferon-alpha therapy on lymphocyte subpopulations in patients with chronic myeloid leukemia'. Together they form a unique fingerprint.

Cite this