Immunoregulatory mechanisms in multiple myeloma.
This review presents current experimental data regarding immunologic changes associated with multiple myeloma (Table 1). It is becoming increasingly clear that some of the immunologic changes are host responses to the malignant plasma cell clone and monoclonal immunoglobulin. In the last 2 to 3 years an anti-idiotypic response has been clearly documented, and cells expressing CD16 and soluble CD16 have been identified as modulators of myeloma cell growth and differentiation. Abnormalities in B- and T-cell differentiation have been observed, most consistently the deficiency of T4 helper cells. Differences in the immunologic changes point to the provocative hypothesis that, in MGUS and the initial stages of myeloma, immunologic responses play an important role in controlling proliferation of the malignant clone, and at some point the system is overwhelmed or fails, leading to an overt or more aggressive disease. The quest is to understand the genesis of the autoregulatory circuits operative in myeloma. Novel strategies for immunotherapy in management of myeloma will arise through improved understanding of host immune response and its cause-and-effect relationship with myeloma cell growth.
Munshi
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NC
Department of Medicine, University of Arkansas for Medical Sciences, Little Rock, USA.
D000361:Agammaglobulinemia / Q000276:immunology; D000818:Animals; D015703:Antigens, CD / Q000276:immunology; D004195:Disease Models, Animal; D006801:Humans; D008214:Lymphocytes / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D009101:Multiple Myeloma / Q000276:immunology*; D010954:Plasmacytoma / Q000276:immunology*
D015703:Antigens, CD