Increasing Tim-3+CD244+, Tim-3+CD57+, and Tim-3+PD-1+ T cells in patients with acute myeloid leukemia

Asia Pac J Clin Oncol. 2020 Jun;16(3):137-141. doi: 10.1111/ajco.13304. Epub 2020 Feb 7.

Abstract

Aim: To characterize the distribution of T cell immunoglobulin mucin-domain-containing-3 (Tim-3) within the exhausted T cells in patients with newly diagnosed acute myeloid leukemia (AML) and AML in complete remission.

Methods: Tim-3 expression and coexpression with PD-1, CD244, and CD57 in CD3+, CD4+, and CD8+T cells were analyzed by multicolored fluorescent flow cytometry in peripheral blood from 28 newly diagnosed, untreated AML patient and 12 cases with AML in complete remission, 23 healthy individuals served as control.

Results: Increasing Tim-3+CD244+ and Tim-3+CD57+ in CD3+, CD4+, and CD8+ T cells were found in AML and AML-CR groups in comparison with healthy controls. Similarly, increasing Tim-3 coexpression PD-1+ CD3+/CD4+/CD8+ T cells were found in AML group. A high tendency of PD-1+Tim-3+CD3+/CD4+/CD8+ T cells was detected in the AML-M4 subtype group followed by the M2 group, and a low tendency was found in the M3 group. Moreover, Tim-3+CD244+CD8+ T cells were found to be significantly higher in the M4 than that in M3 group. Dynamic changes of Tim-3+ T cells in AML patients who achieved CR after chemotherapy at different time points showed that Tim-3+ T cell subsets were evidently decreased; however, they remained at a higher level in most AML-CR patients.

Conclusion: We made a novel observation on distribution of Tim-3+CD244+, Tim-3+CD57+, and Tim-3+PD-1+ T cells in patients with AML. Chemotherapy is incapable of resolving immunosuppression in some cases with AML in CR status.

Keywords: AML; PD-1; Tim-3; T cell exhaustion; T cell subset.

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • CD57 Antigens / genetics*
  • Child
  • Female
  • Humans
  • Leukemia, Myeloid, Acute / genetics*
  • Leukemia, Myeloid, Acute / pathology
  • Male
  • Middle Aged
  • Programmed Cell Death 1 Receptor / genetics*
  • Signaling Lymphocytic Activation Molecule Family / genetics*
  • Young Adult

Substances

  • CD244 protein, human
  • CD57 Antigens
  • Programmed Cell Death 1 Receptor
  • Signaling Lymphocytic Activation Molecule Family