SU-DHL-1

MoAbs Against SU-DHL-1 Cells Bind to Peripheral Blood Mononuclear Cells and Normal Lymphoid Tissues

Three murine monoclonal antibodies (MoAbs), named 2H9, 1E9, and 1A2, were produced after immunization of BALB/c mice with cells of the SU-DHL-1 cell line from a true histiocytic lymphoma. None of the three MoAbs reacted with B or T lymphocytes in the peripheral blood or lymphoid tissues such as lymph nodes, tonsils, and spleens. Antibodies 1E9 and 2H9 stained monocytes in peripheral blood. The former elicited an intracytoplasmic punctate reaction (Fig. 1A), whereas the latter produced nuclear membrane staining of variable intensity (Fig. 1D); 1E9 also reacted with the cytoplasm of granulocytes (Fig. 1A, arrow), whereas 1A2 did not react with either monocytes or granulocytes.

In normal lymphoid tissues, including tonsils and lymph nodes, 1E9 and 2H9 were very similar in their staining pattern; both reacted with the nuclear membranes of histiocytes and IR cells (Fig. 1B and E). This reactivity with IR cells was confirmed by examining lymph nodes from two patients with dermatopathic lymphadenitis, which contained abundant IR cells (Fig. 1C). Antibody 1A2 reacted only with rare cells scattered in the lymphoid tissue (Fig. 1F).

Fig. 1 (A) 1E9 staining of a smear of a monocyte-enriched fraction of PBL, (B) a frozen section of a tonsil, and (C) a frozen section of a lymph node from a patient with dermatopathic lymphadenitis. (D) 2H9 staining of a smear of a monocyte-enriched fraction of PBL and (E) a frozen section of a tonsil. (F) 1A2 reacts with rare cells in a section of the tonsil. (Hsu SM, et al., 1986)

NKILA Was a Tumor Suppressor lncRNA in SU-DHL-1 Cells

The long non-coding RNA (lncRNA) NKILA, localized to 20q13.31, is a negative regulator of NF-κB signaling implicated in carcinogenesis. As a CpG island is embedded in the promoter region of NKILA, it is hypothesized as a tumor suppressor lncRNA silenced by promoter DNA methylation in non-Hodgkin's lymphoma (NHL). The tumor suppressor function of NKILA in lymphoma was further explored by examining cell proliferation and cell death in SU-DHL-1 cells that were completely unmethylated for NKILA. The knockdown of NKILA led to a significantly increased cell proliferation rate compared with the control (Fig. 2A). Furthermore, the knockdown of NKILA resulted in reduced cell death in SU-DHL-1 cells (Fig. 2B). These results supportively indicated that NKILA acted as a tumor suppressor lncRNA in SU-DHL-1 cells.

Fig. 2 NKILA suppresses cell growth and promotes cell death in SU-DHL-1. (Zhang MY, et al., 2022)