Ecto-5′-Nucleotidase (E5′-NT, 27.2, CD73), 27.1, Leu13, CD28 and LAM-1(Leu8) Antigens in Mycosis Fungoides (MF)

Abstract

Two monoclonal antibodies (MoAbs) B121 and B124 to the human lymphocyte differentiation antigen E5′-NT (CD73), and the MoAbs 27.2 and 27.1 that were raised to HTLV-1+CD4+CD25+ leukemic T cells were tested immunohistochemically on frozen sections of 13 cases of MF together with Leu13, CD28, LAM-1(Leu8) and other standard T-cell markers. Controls included 7(5T, 2B) non-MF cutaneous non-Hodgkin's lymphomas (NHL), 2 cutaneous T lymphoid leukemias (T-ALL), 13 miscellaneous non-neoplastic dermatoses, 11(5T, 6B) extracutaneous NHL, and 5 splenic B-hairy cell leukemias. Previous studies suggest that 27.2 also recognizes the CD73 antigen and is present in high density in some cases of HTLV-1+ adult thymic leukemia/lymphoma (ATL) and HTLV-1- Sezary syndrome (Y. Fukunaga et al., Blood 74:2486-2492, 1989). In the studies reported here B121, B124 and 27.2 reacted similarly with the MF and control samples tested. The CD73 antigen was present in the majority of lymphoid cells from 8 (62%) of 13 cases of MF. In one of these cases the CD73 antigen was detected only in the deeper and more pleomorphic MF dermal infiltrate. Although CD73 expression was noted in varying numbers of lymphocytes from many of the control benign and malignant lymphoproliferative lesions of the skin, none of the extracutaneous NHL or HCL cases tested showed significant numbers of CD73+ cells. Ten, 11 and 11 of the 13 MF cases also showed moderate to high numbers of cells reactive with 27.1, Leu13 and CD28, respectively. Most of the MF cases also showed moderate to high co-expression of βF1 (TCRβ), CD3 and CD4, and 9 cases showed moderate numbers of CD8+ cells as well. In contrast to the control dermatoses, where significant co-expression of the majority T-cell markers LAM-1(Leu8), CD5 and CD7 was the rule, 11 of the 13 MF cases showed significant loss of one or more of these antigens. One or more of these antigens was notably also lost with CD73 in 3 patients who had, or developed, systemic MF. The above results indicate that MF cases often co-express the CD73/27.2 antigen with 27.1, Leu13, CD28, βF1 (TCRβ), CD3 and CD4, and may show a concurrent absence of CD5, CD7 or LAM-1(Leu8) antigens with or without loss of CD73. The possible roles of CD73, Leu 13, CD28 and LAM-1(Leu8) in controlling cell proliferation, adhesion and migration in MF are discussed.