Beta 2-microglobulin amyloidosis: role of monocytes/macrophages.
OBJECTIVE
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.


RESULTS
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.


CONCLUSIONS
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.
Hou
Fan Fan
FF
Division of Nephrology, Nanfang Hospital, Guangzhou, People's Republic of China. ffhou@public.guangzhou.gd.cn
Owen
William F
WF
D000686:Amyloidosis / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D008264:Macrophages / Q000502:physiology*; D009000:Monocytes / Q000502:physiology*; D001613:beta 2-Microglobulin / Q000378:metabolism*
D001613:beta 2-Microglobulin