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Amyloid A (AA) amyloidosis is a serious complication of chronic inflammatory, infectious and neoplastic diseases (Merlin & Bellotti, 2003). Insoluble amyloid fibril deposition resulting from the extracellular aggregation of proteolytic fragments of serum amyloid A (SAA), an acute-phase reactant protein, causes progressive deterioration in various organs (Obici et al., 2009; Perfetto et al., 2010). Moreover, long-term overproduction of the SAA protein is a key component of the resultant pathogenetic cascade (Pettersson et al., 2008). Recent fundamental analyses of SAA gene activation have revealed that proinflammatory cytokines such as IL-1β, TNFα and IL-6 are key players in SAA synthesis, leading to speculation that biological modifiers to block the activity of these cytokines may function as novel therapeutic drugs for AA amyloidosis. Some reports have dealt with the beneficial clinical effects of the IL-1 receptor antagonist, TNF inhibitors, and IL-6 receptor antibody (ab) on AA amyloidosis. In this chapter, we present evidence that tocilizumab, a humanized anti-interleukin-6 receptor ab, is a powerful inhibitor of SAA production and has the potential of becoming a first-line drug for AA amyloidosis.

Tocilizumab for the Treatment of AA Amyloidosis