Analysis of abnormal preduction of C3 by psoriatic kerafinocyte and its control by ultraviolet irradiation

银屑病角化细胞C3异常生成分析及紫外线照射控制

• 批准号: 09670865
• 负责人: TERUI Tadashi
• 金额: $ 2.24万
• 依托单位: Tohoku University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1997
• 资助国家: 日本
• 起止时间: 1997 至 1998
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09670865/
• 关键词: complement; C3; psoriasis; ultraviolet; UVB; UVA; PUVA; UVB erythemq

The present study was designed to investigate by using ELISA and RT-PCR methods whether PUVA or UVB treatment affects C3 production byIFNgamma-stimulated keratinocytes cultured in serum-free medium. The results showed that PUVA and UVA reduced the C3 production by IFNgamma-stimulatedepidermal keratinocytes dose-dependently, although the effect of PUVA was stronger than that of UVA alone. Interestingly, UVB induced an enhancement of the C3 production at lower doses ranging from 10 to 50 mJ/cm^2, while it reduced the production at higher doses of 75 and 100 mJ/cm^2. This phenomenon was found at both the protein and mRNA level. In every experiment, changes in C3 mRNA levels preceded those of its protein levels. In our experimental system, PUVA, UVA, or UVB treatment did not affect theC3 production without IFNgamma-stimulation. The observations of our present study suggest that a reduction of the C3 production by PUVA or UVA treatment may explain in part why PUVA is effective in the treatment of inflammatory dermatoses such as psoriasis and other sterile pustular dermatoses, and the results of the UVB experiments may explain why there are both pro-inflammatory and anti-inflammatory effects.

本研究采用ELISA法和RT-PCR法研究了PUVA和UVB对无血清培养的角质形成细胞经干扰素刺激后C3产生的影响。结果表明，PUVA和UVA均可剂量依赖性地抑制IFN-γ刺激真皮角质形成细胞产生的C3，但PUVA的作用强于单独UVA。有趣的是，UVB在10~50mJ/cm2的低剂量下可促进C3的产生，而在75mJ/cm2和100mJ/cm2的较高剂量下则抑制C3的产生。这种现象在蛋白质和mRNA水平上都存在。在每个实验中，C3mRNA水平的变化先于其蛋白质水平的变化。在我们的实验系统中，PUVA、UVA或UVB处理不影响C3的产生，而没有IFN伽马刺激。我们目前的研究表明，PUVA或UVA治疗减少C3的产生可能部分解释了为什么PUVA在治疗银屑病和其他无菌脓疱性皮肤病等炎症性皮肤病方面有效，而UVB实验的结果可能解释了为什么PUVA既有促炎作用，又有抗炎作用。

项目成果

Terui T, Tagami H.: "Annular elastolytic sarcoidosis of the face" European Journal Dermatology. 8・2. 127-129 (1998)

Terui T, Tagami H.：“面部环形弹性松解性结节病”，欧洲皮肤病学杂志 8・2（1998 年）。

Tabata N,Tagami H,Terui T.: "Dehydroepiandrosterone may be one of the regulators of cytokine production in atopic dermatitis." Archives of Dermatological Research. 289・8. 410-414 (1997)

Tabata N, Tagami H, Terui T.：“脱氢表雄酮可能是特应性皮炎中细胞因子产生的调节剂之一。”皮肤病学研究档案 289・8 (1997)。

Terui T,Aiba S,Tagami H.: "Solitary subcutaneous mucinosis surrounded by bizarre-shaped, factor XIIIa-positive cells with intranuclear vacuoles." J Cutan Pathol. 25. 271-274 (1998)

Terui T、Aiba S、Tagami H.：“孤立的皮下粘蛋白沉积症，周围环绕着形状怪异、带有核内空泡的 XIIIa 因子阳性细胞。”

Ozawa M,Terui T,Tanita M,Kato T,Tagami H.: "Release of monocyte chemoattractants by polymorphonuclear leukocytes stimulated by their adhesion to stratum corneum opsonized via complement activation, measured with a human acute monocyte leukemic cell line,

Ozawa M、Terui T、Tanita M、Kato T、Tagami H.：“多形核白细胞通过补体激活调理角质层粘附，刺激其释放单核细胞趋化剂，用人类急性单核细胞白血病细胞系测量，

Terui T, Hirao T, Sato Y,他7名: "An increased ration of interleukin-1 receptor antagonist to interleukin-1α in inflammatory skin diseases." Expental Dermatology. 7・6. 327-334 (1998)

Terui T、Hirao T、Sato Y 和其他 7 人：“炎症性皮肤病中白细胞介素 1 受体拮抗剂与白细胞介素 1α 的比例增加。” 7·6 (1998)。