Roles of Immunoglobulins in Amyloidogenesis in Cutaneous Nodular Amyloidosis

Ito, Kei; Hashimoto, Ken; Kambe, Naoto; Van, Shirley

doi:10.1111/1523-1747.ep12471778

Cited by 23 publications

(13 citation statements)

References 26 publications

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“…4-7], Ito et al [6] reported that immunoglobulins and complements were found in amy loid deposits using a direct immunofluorescence method as our results show. They suggested that X light chain was an inherent component of amyloid fibrils, whereas other chains and complement represented nonessential absorp tion on amyloid material, since other components except a. light chain could be washed out by pretreatment of sec tions with some detergents.…”

Section: Discussionsupporting

confidence: 76%

Primary Localized Cutaneous Nodular Amyloidosis: Case Report and Biochemical Analysis of Amyloid

et al. 1991

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We report a patient with scalp lesions of primary localized cutaneous nodular amyloidosis. The extensive examination revealed no systemic involvement. Analysis of glycosaminoglycans (GAGs) in amyloid deposits showed a twofold increase as compared with normal skin, which was due to the increase in dermatan sulfate. Local disorders of GAG metabolism may be related to the amyloid fibril formation. Amyloid fibrils were purified and identified electron-microscopically, which consisted of two major 12,000- and 13,000-dalton and minor 29,000- and 48,000-dalton peptides. Western blotting analysis showed a minor 29,000-dalton peptide reactive with antibodies against both κ and λ light chains of immunoglobulin. There is a possibility that some components of amyloid in some cases of primary localized cutaneous nodular amyloidosis may consist of both κ and λ immunoglobulin light chains.

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Section: Discussionsupporting

confidence: 76%

Primary Localized Cutaneous Nodular Amyloidosis: Case Report and Biochemical Analysis of Amyloid

et al. 1991

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“…The presence of early complement factors C1q and C3 has been described in lichen amyloidosis [61,62], several forms of renal amyloidosis [63,64] and amyloid AL neuropathy [65]. The authors of these studies state that the relevance of these complement factors for the formation of the amyloid deposits is yet unclear, but they suggest that their presence represents probably a nonessential absorption and that amyloid material could act as a filamentous sponge [62,66]. In a recent study, we found C3 in a broad variety of amyloid diseases.…”

Section: Microgliamentioning

confidence: 99%

The Neuroinflammatory Response in Plaques and Amyloid Angiopathy in Alzheimers Disease: Therapeutic Implications

2005

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The amyloid plaques in Alzheimer's disease (AD) brains are co-localised with a broad variety of inflammation-related proteins (complement proteins, acute-phase proteins, pro-inflammatory cytokines) and clusters of activated microglia. The present data suggest that the Abeta depositions in the neuroparenchyma are closely associated with a locally-induced, non-immune-mediated chronic inflammatory response. Clinicopathological and neuroradiological data show that activation of microglia are a relatively early pathogenic event that precedes the process of severe neuropil destruction in patients. Recent gene findings (cDNA microarray) confirm the immunohistochemical findings of an early involvement of inflammatory and regenerative pathways in AD pathogenesis. Abeta deposition, inflammation and regenerative mechanisms are also early pathogenic events in transgenic mice models harbouring the pathological AD mutations, while "later" neurodegenerative characteristics are not seen in these models. Next to the plaques, Abeta amyloid deposition is frequently found in the walls of cerebral vessels (cerebral amyloid angiopathy). Most common is the type of amyloid deposition in the walls of meningeal and medium-sized cortical arteries, and more rarely, microcapillary amyloid angiopathy (dyshoric angiopathy). Immunohistochemical studies show that in AD patients, the majority of the amyloid deposits in the walls of the larger vessels is not associated with a chronic inflammatory response in contrast to micro-capillary amyloid angiopathy. In this contribution, we will give an overview of the similarities and differences between the involvement of inflammatory mechanisms in vascular and plaque amyloid in AD and transgenic models. The implications of the reviewed studies for an inflammation-based therapeutical approach in AD will be discussed.

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“…The exact mechanism of NA remains unclear. Gene rearrangement studies have confirmed clonality ofthe amyloid-producing plasma cells in the skin, but not in the bone marrow, and suggested that NA might arise from local plasma cell dyscrasia or plasmacytoma (1). Several disorders, including systemic sclerosis, primary biliary cirrhosis, systemic lupus erythematosus, Sjogren's syndrome, and rheumatoid arthritis, have been associated with NA (2).…”

Section: Discussionmentioning

confidence: 99%

“…Amyloid in the skin may be derived directly from keratinocj^es, or secondarily fi'om immunoglobulin light chain fi-agments (AL type), fragments ofthe acute-phase reactant serum amyloid A (AA type), etc. Nodular amyloidosis (NA) is a rare type of localized AL amyloidosis, with most reported cases being ofthe lambda light chains (1) and is often histopathologically indistinguishable from systemic amyloidosis. Its association with lymphoma has been observed infi-equently.…”

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confidence: 99%

Localized AL Amyloidosis in a Patient with Diffuse Large B-cell Lymphoma of the Breast

Chiu¹,

Chu²,

Tsai³

2012

Acta Derm Venerol

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Roles of Immunoglobulins in Amyloidogenesis in Cutaneous Nodular Amyloidosis

Cited by 23 publications

References 26 publications

Primary Localized Cutaneous Nodular Amyloidosis: Case Report and Biochemical Analysis of Amyloid

Primary Localized Cutaneous Nodular Amyloidosis: Case Report and Biochemical Analysis of Amyloid

The Neuroinflammatory Response in Plaques and Amyloid Angiopathy in Alzheimers Disease: Therapeutic Implications

Localized AL Amyloidosis in a Patient with Diffuse Large B-cell Lymphoma of the Breast

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