Enhanced Production Of Interleukin‐1 And Tumor Necrosis Factor α By Cultured Peripheral Blood Monocytes From Patients With Scleroderma

Umehara, Hisanori; Kumagai, Shunichi; Murakami, Masao; Suginoshita, Toshihiko; Tanaka, K.; Hashida, Seiichi; Ishikawa, Eiji; Imura, Hiroo

doi:10.1002/art.1780330619

Cited by 40 publications

(21 citation statements)

References 10 publications

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“…Esses dados sugerem que a osteopenia em mãos, na esclerodermia sistêmica, está associada mais a fenô-menos regionais, tais como tendência à imobilidade causada pela fibrose dérmica, isquemia crônica decorrente da endarterite obstrutiva da microcirculação e reabsortiva local [35][36][37] do que a qualquer alteração sistêmica propriamente dita.…”

Section: Discussionunclassified

“…Além disso, a síntese de TGF-β é fortemente estimulada pelo fator de crescimento derivado de plaquetas (PDGF), que se encontra elevado no soro de pacientes com esclerodermia 43 . Por outro lado, certas citocinas, como a interleucina 1 (IL-1) e o fator de necrose tumoral alfa (TNF-α), que aumentam a reabsorção óssea, são encontradas nos locais de maior atividade da doença 37,39 , o que justificaria o encontro radiológico de osteopenia e osteólise regionais (mãos, pés, ramo da mandíbula, costelas, etc.). Entretanto, as citocinas mencionadas não teriam ação sistêmica em nível ósseo, visto que os níveis séricos estão normais em pacientes com esclerodermia sistêmica 39 .…”

Section: Discussionunclassified

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Estudo da densidade óssea na esclerodermia sistêmica

Silva¹,

Szejnfeld²,

Assis³

et al. 1997

Rev. Assoc. Med. Bras.

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INTRODUÇÃOO envolvimento ósseo, em pacientes com esclerodermia sistêmica, caracteriza-se, geralmente, por reabsorção óssea, predominantemente das extremidades das falanges distais dos dedos das mãos e, mais raramente, dos pés e outras partes do esqueleto [1][2][3] . Também, já foi descrito, em pacientes com esclerodermia, principalmente em mãos, osteopenia localizada periarticular, que, nos estágios mais tardios da doença, pode estender-se por todo o membro comprometido [4][5][6] . A observação inicial, associando osteopenia generalizada à esclerodermia, foi feita por Serup et al.

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Section: Discussionunclassified

Estudo da densidade óssea na esclerodermia sistêmica

Silva¹,

Szejnfeld²,

Assis³

et al. 1997

Rev. Assoc. Med. Bras.

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“…Fither IL-1 or concanavalin A (Con A) was reported to induce active TGF-/3 from purified T cells without the proliferative response, although a coexistence of both stimulations did not induce it [22]. The enhanced production of TGF-/J from MNC of SSc might come from inadequate T cell stimulation during AMLR, because SSc monocytes were shown to produce higher levels of IL-1 [7].…”

Section: Discussionmentioning

confidence: 99%

“…Among them, cytokines such as IL-1 and tumour necrosis factor-alpha (TNF-tt) which induce the proliferation of fibroblasts and/or the synthesis of collagens have been suggested to play a key role in the fibrotic mechanism of SSc. We previously reported the hyperproduction of IL-1 and TNF-ci by monocytes of SSc patients [7]. Recently, TGF-/3 has been shown to induce fibroblasts to increase extracellular matrix production (8,9], and is also thought to be deeply involved in ihe fibrosis of SSc.…”

Section: Introductionmentioning

confidence: 96%

Enhanced production of transforming growth factor-beta (TGF-β) during autologous mixed lymphocyte reaction of systemic sclerosis patients

Ôta

Kumagai

Morinobu

et al. 1995

Clinical and Experimental Immunology

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SUMMARY Systemic sclerosis (SSc) is characterized by systemic fibrosis and microvascular lesions. As TGF‐β is suggested to be related to skin fibrosis, we examined the production of TGF‐β from peripheral mononuclear cells (MNC) of SSc patients. Since anti‐TGF‐β neutralizing antibody improved the defective proliferative response in autologous mixed lymphocyte reaction (AMLR) of SSc patients, TGF‐β was thought to participate in the decreased AMLR of SSc patients. Greater amounts of TGF‐β in the active as well as in the latent forms were produced during AMLR of SSc patients than that of normal subjects. It was suggested that TGF‐β excessively produced from the MNC of SSc patients might play a major role in the fibrosis of the patients during AMLR‐like in vivo responses.

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“…The clinical association or 'overlap' of scleroderma with other autoimmune connective tissue diseases such as systemic lupus erythematosus and polymyositis [1], together with its high incidence of distinctive autoantibodies [2,3], circulating immune complexes [4,5] and evidence of T cell activation [6] with elevated levels of cytokines [7,8], all strongly suggest that autoimmune mechanisms are involved in the pathogenesis of the disease. The development of scleroderma-like lesions as a feature of chronic graft-versus-host disease, both experimentally [9] and in man [10], further supports this concept.…”

Section: Introductionmentioning

confidence: 99%

Antibodies to membranes of endothelial cells and fibroblasts in scleroderma

Hill¹,

Phipps²,

Cartwright

et al. 1996

Clinical and Experimental Immunology

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SUMMARYAnti-endothelial and other cell membrane-reactive antibodies in scleroderma were characterized by immunoblotting sera with membrane and cytosol preparations of human umbilical vein endothelial cells (HUVEC), dermal fibroblasts and a T cell lymphoma HUT78. Antibodies reactive with HUVEC membranes were found in 17 of 20 patients with scleroderma (33 bands) in contrast to only two of 20 controls (two bands; P<0 . 01) and three of 11 patients with myocardial infarction (four bands). Eleven of the 20 patients possessed antibodies that were specific for HUVEC membrane and did not cross-react with other cell lines. Analysis of patient subgroups showed that HUVEC membrane antibodies were present in nine of 11 patients with systemic sclerosis and in all nine with the CREST syndrome, and were HUVEC-specific in five and six of these cases, respectively. Although considerable heterogeneity was seen, antibodies to an 18-19-kD membrane epitope were found in 11 of the 20 patients but in none of the controls (P<0 . 01). This antibody which reacted particularly with HUVEC (n 9) and HUT78 membranes (n 9) was associated with CREST syndrome rather than systemic sclerosis (9/9 versus 1/ 11; P<0 . 01), and after elution was shown to possess anticentromere activity. In addition, antibodies reactive with both fibroblast (n 11; 18 bands) and HUT78 membranes (n 18; 42 bands) were detected and were specific for either fibroblast or HUT78 membranes in nine and 14 patients, respectively. There was no significant difference in the incidence of these fibroblasts and HUT78 membrane antibodies in the two patient subgroups. These findings support the concept that membranereactive antibodies, including anticentromeric antibodies, may play a central role in the pathogenesis of scleroderma, through their ability to react with endothelial cells.

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Enhanced Production Of Interleukin‐1 And Tumor Necrosis Factor α By Cultured Peripheral Blood Monocytes From Patients With Scleroderma

Cited by 40 publications

References 10 publications

Estudo da densidade óssea na esclerodermia sistêmica

Estudo da densidade óssea na esclerodermia sistêmica

Enhanced production of transforming growth factor-beta (TGF-β) during autologous mixed lymphocyte reaction of systemic sclerosis patients

Antibodies to membranes of endothelial cells and fibroblasts in scleroderma

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