Premium
Expression of interleukin‐1β and tumour necrosis factor‐α in plasma cells from patients with multiple myeloma
Author(s) -
Sati Hamdi I. A.,
Greaves Mike,
Apperley Jane F.,
Russell R. Graham G.,
Croucher Peter I.
Publication year - 1999
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1999.01193.x
Subject(s) - multiple myeloma , tumor necrosis factor alpha , cancer research , medicine , plasma cell myeloma , interleukin 1β , interleukin , plasma cell neoplasm , plasma cell , interleukin 6 , necrosis , pathology , cytokine , immunology , plasmacytoma
Interleukin‐1β (IL‐1β) and tumour necrosis factor‐α (TNF‐α) are potent bone resorbing cytokines that may contribute to the development of the osteolytic bone disease observed in patients with multiple myeloma (MM). Although these factors have been identified in cultures of bone marrow mononuclear cells isolated from patients, the identity of the cells responsible for producing IL‐1β and TNFα remains unclear. Using a sensitive dual‐colour fluorescence in situ hybridization (FISH) technique and a two‐colour immunofluorescence method we have investigated the expression of the mRNA and protein, for IL‐1β and TNFα, by individual bone marrow plasma cells from patients with MM and monoclonal gammopathy of undetermined significance (MGUS). The mRNA for IL‐1β and TNFα was identified in all cells expressing the immunoglobulin light chain from all patients with MM and MGUS. However, the IL‐1β protein could not be detected in cytoplasmic light chain positive cells in any of the patients examined. In contrast, the TNFα protein was detected in clonal plasma cells from patients with both MM and MGUS. Interestingly, the IL‐1β and TNFα mRNA and proteins were readily detected within a small proportion of the non‐plasma cells from patients with both MM and MGUS. These data suggest that myeloma cells in vivo are able to produce TNFα but not IL‐1β. In addition, a small proportion of accessory cells are likely to be able to contribute to the production of both IL‐1β and TNFα.