Autoantibodies against matrix metalloproteinase-1 in patients with localized scleroderma

Tomimura, Saori; Ogawa, Fumihide; Iwata, Y.; Komura, Kazuhiro; Hara, Toshihide; Muroi, Eiji; Takenaka, Motoi; Shimizu, Kazuhiro; Hasegawa, Minoru; Fujimoto, Manabu; Sato, Shinichi

doi:10.1016/j.jdermsci.2008.04.013

Cited by 38 publications

(31 citation statements)

References 24 publications

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“…72 Anti-MMP1 antibodies are not seen in normal healthy controls or in patients with SLE or dermatomyositis and therefore may be sclerosis-specific. 72 The small molecule GTPase Rac1, known to be involved in cell trafficking and migration, may be a key component in the persistence of myofibroblasts seen in morphea lesions. 73 Insulin-like growth factor (IGF) may also be important in the pathogenesis of morphea.…”

Section: Molecular Pathogenesis Key Pointsmentioning

confidence: 99%

“…71 The inhibition of collagen breakdown may be partially mediated by anti-MMP antibodies. 72 Patients with morphea and systemic sclerosis have autoantibodies that are capable of inhibiting MMP1 collagenase activity. 72 Anti-MMP1 antibodies are not seen in normal healthy controls or in patients with SLE or dermatomyositis and therefore may be sclerosis-specific.…”

Section: Molecular Pathogenesis Key Pointsmentioning

confidence: 99%

“…72 Patients with morphea and systemic sclerosis have autoantibodies that are capable of inhibiting MMP1 collagenase activity. 72 Anti-MMP1 antibodies are not seen in normal healthy controls or in patients with SLE or dermatomyositis and therefore may be sclerosis-specific. 72 The small molecule GTPase Rac1, known to be involved in cell trafficking and migration, may be a key component in the persistence of myofibroblasts seen in morphea lesions.…”

Section: Molecular Pathogenesis Key Pointsmentioning

confidence: 99%

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Update on morphea

Fett

Werth

2011

Journal of the American Academy of Dermatology

334

197

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Section: Molecular Pathogenesis Key Pointsmentioning

confidence: 99%

Section: Molecular Pathogenesis Key Pointsmentioning

confidence: 99%

Section: Molecular Pathogenesis Key Pointsmentioning

confidence: 99%

See 1 more Smart Citation

Update on morphea

Fett

Werth

2011

Journal of the American Academy of Dermatology

334

197

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“…Antibodies to fibrillin 1 have been detected in both morphea [8] and scleroderma [9] as have antibodies to matrix-metalloprotein-1 (MMP-1) which inhibit collagenase activity [10].…”

Section: Aetiologymentioning

confidence: 99%

Dissecting the enigma of scleroderma: possible involvement of the kynurenine pathway

Noakes

2017

Pteridines

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“…Additionally, soma cases of induced type SSc in multiple sclerosis patients treated with INF-γ were found [28,31]. Moreover, intensified deposition of extracellular matrix components, including collagen I and III, fibronectin, glycosaminoglycans depends on their intensified production and, on diminished decomposition by matrix metalloproteinases [14,[32][33][34][35].…”

Section: Pathogenesis Of Sclerodermamentioning

confidence: 99%

Role of UVA1 phototherapy in treatment of scleroderma and scleroderma-like disorders”

Osmola‐Mańkowska¹,

Dańczak‐Pazdrowska²,

Olek‐Hrab³

et al. 2012

cejoi

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Treatment of scleroderma and scleroderma-like diseases poses a serious challenge to contemporary dermatology due to the complexity of its pathogenesis, low incidence of the diseases and their heterogenous clinical expression. the manifestation of this autoimmune disease includes an increased production and deposition of collagen fibres types I and III in the skin and connective tissue as well as vascular alterations. Ultraviolet A1 (UVA1) phototherapy affects various stages of a morbid process in scleroderma: it inhibits inflammation and affects the consequences of it, fibrosis. Currently, UVA1 is proposed as a potential treatment and is believed to have a multifold mechanism of action. This includes, inducing apoptosis in T and B lymphocytes, inhibition of proinflammatory cytokine production and ability to induce collagenase production by fibroblasts. UVA1 irradiation may also interact with endothelial cells, promoting angiogenesis. Efficacy of high, moderate, and low doses of UVA1 was documented. Advantages of UVA1 phototherapy include the evident avoidance of systemic side effects of psoralens such as nausea and vomiting or photokeratitis as well as lower risk of phototoxic reactions with deeper penetration of radiation. Its disadvantages include high cost of equipment, thus reducing the accessibility of the treatment to specialized centres. Due to its unique mechanism of action, attempts to useUVA1 phototherapy seem justified in other rare diseases, developing with skin induration.

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Autoantibodies against matrix metalloproteinase-1 in patients with localized scleroderma

Abstract: Background. Localized scleroderma (LSc) is characterized by cutaneous fibrosis and various

Cited by 38 publications

References 24 publications

Update on morphea

Update on morphea

Dissecting the enigma of scleroderma: possible involvement of the kynurenine pathway

Role of UVA1 phototherapy in treatment of scleroderma and scleroderma-like disorders”

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