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  • Title: Beta 2-microglobulin amyloidosis: role of monocytes/macrophages.
    Author: Hou FF, Owen WF.
    Journal: Curr Opin Nephrol Hypertens; 2002 Jul; 11(4):417-21. PubMed ID: 12105392.
    Abstract:
    PURPOSE OF REVIEW: Macrophage infiltration is a distinctive histological characteristic of beta2-microglobulin amyloidosis. Studies reported during the past years have helped to clarify the role of monocytes/macrophages in the fibrillar precipitation of beta2-microglobulin and in the pathogenesis of osteoarticular pathology. RECENT FINDINGS: Contrary to the original view, macrophage infiltration is more likely a secondary phenomenon of amyloidosis rather than an initiating event. The observation that macrophages are associated with a later stage of beta2-microglobulin amyloidosis suggests a possible role of these cells in transformation of clinical silent deposits into symptomatic osteoarticular destruction. Accumulating evidence suggests that beta2-microglobulin modified with advanced glycation end products plays a key role in recruitment and activation of macrophages through an advanced glycation end products receptor-mediated pathway, and thus may contribute to the development of local cellular inflammation in beta2-microglobulin amyloidosis. SUMMARY: Beta 2-microglobulin amyloidosis arthropathies may result from progressive accumulation of advanced glycation end products in long-lived amyloid linked to a heightened cellular response. Antagonism of the interaction between advanced glycation end products and their receptor may be a relevant strategy for cellular inflammation in beta2-microglobulin amyloidosis.
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