Autologous T lymphocytes can be employed for immune therapy of patients with acute myeloid leukemia (AML). In an earlier study (

Biol Blood Marrow Transplant 2002; 8:557
), we found that AML cells can be used as antigen presenting cells to activate and expand T cells in culture with IL-2 and monoclonal antibody (mAb) to CD3. In this study, we found that a substantial proportion of the expanded T cells expressed CD33 (34 ± 16%; range: 8 – 58%; N=11) and CD13 (26 ± 5%; range: 22 – 33%), but not CD14. It is unlikely that the myeloid markers were absorbed onto the activated T cells, since the same expression pattern was observed in cultures with purified T cells from normal donors. A literature review disclosed two reports that also observed co-expression of CD33 on activated T cells from both AML patients and normal controls (
Schmidt-Wolf et al, Br J Haematol. 1995; 90:512
;
Nakamura et al, letter in Blood, 1994; 83:1442
). We measured the functional capacity of the activated T cells in a 4-hr Cr-51 release assay. Pre-incubation of the T cells with anti-CD33 mAb and/or anti-CD13 mAb did not change the cytotoxicity against AML cells. Also, killing of AML cells was not affected by the depletion of CD33+ or CD13+ activated T cells using magnetic beads. The activated T cells migrated in a chemotactic response to a peptide analog (CTCE-0214) of Stromal cell derived factor-1 (SDF-1) when measured in a trans-well assay. When activated T cells were pre-incubated with anti-CD33 mAb, enhanced chemotaxis was observed in response to CTCE-0214 (39.9 ± 0.5% vs 26.9 ± 0.3%, p < 0.001). However, incubation with anti-CD13 mAb did not change the proportion of chemotactic cells. The results of this study confirmed that myeloid antigens can be induced on activated T cells from patients with AML and that there are differences in the mobility of CD33+ T cells in the presence of a chemotactic molecule. Further study of the biological significance of CD33 expression on activated T cells in AML and other diseases is warranted.

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