물방울양 건선과 판상 건선에서 Heat Shock Protein 60과 T 세포 수용체 γδ의 발현 (Expression of 60kd Heat Shock Protein and T Cell Receptor γδ in Guttate and Plaque Psoriasis)

서지정보

· 발행기관 : 대한피부과학회
· 수록지 정보 : 대한피부과학회지 / 46권 / 1호 / 26 ~ 33페이지
· 저자명 : 김현준, 박은주, 김철우, 조희진, 김광호, 김광중, 박혜림, 김용선

초록

Background: Psoriasis is a chronic disease of the skin that appears to be of autoimmune nature. An association with throat streptococcal infections in some subtypes of psoriasis has been suggested. Heat shock protein (HSP) is known to play an important role in the immune and inflammatory responses of the skin including psoriasis. Recent studies have suggested that T-cell receptor (TCR) responds to HSP peptides.
Objective: We aimed to investigate the role and correlation of HSP and TCR in the pathogenesis of guttate psoriasis by studying whether there is any difference in HSP60 and TCR γδ-positve cell expression in guttate psoriasis compared to plaque psoriasis.
Methods: Skin biopsy specimens from patients with guttate psoriasis (n=12), patients with plaque psoriasis (n=12), and normal skin controls (n=5) were used in the study. One-half were fixed in formalin and embedded in paraffin, and the other half were snap frozen and stored. Antibodies to HSP60 and TCRγδ were applied immunohistochemically. An immunoreactivity intensity distribution index (IRIDI) of HSP was calculated to express the proportion of the immunoreactive cells as well as the staining intensity in different layers of the epidermis. And the expression of HSP60 was also analyzed by Western blot analysis. TCRγδ-positive cell counts were semiquantitatively evaluated in 3 consecutive X400 microscopic fields, which were divided into epidermis and dermis.
Results: The mean IRIDI scores for HSP60 expression of guttate psoriasis were moderately higher than those for normal skin in the suprabasal layer (p＜0.05), but not significantly different from normal in the other layers and plaque psoriasis. And results from Western blot analysis were similar to the mean total IRIDI scores for HSP60 expression, but there was not significant differentiation amongst the three groups. TCRγδ-positive cell counts in the lesions of guttate and plaque psoriasis were significantly different from normal skin (p＜0.05) and TCRγδ-positive cell counts for guttate psoriasis were higher compared to those for plaque psoriasis (p＜0.05). There was no significant correlation between HSP60 and TCRγδ (p＞0.05).
Conclusion: This study suggests that up-regulation of HSP60 expression in the suprabasal layer may support the association of HSP60 in the etiology of psoriasis. TCRγδ may be involved in the pathogenesis of psoriasis, especially guttate psoriasis rather than plaque psoriasis, even though the correlation of HSP60 and TCRγδ was not significant. The mechanism of how they act to promote induction and aggravation in psoriasis remains to be elucidated.

영어초록

Background: Psoriasis is a chronic disease of the skin that appears to be of autoimmune nature. An association with throat streptococcal infections in some subtypes of psoriasis has been suggested. Heat shock protein (HSP) is known to play an important role in the immune and inflammatory responses of the skin including psoriasis. Recent studies have suggested that T-cell receptor (TCR) responds to HSP peptides.
Objective: We aimed to investigate the role and correlation of HSP and TCR in the pathogenesis of guttate psoriasis by studying whether there is any difference in HSP60 and TCR γδ-positve cell expression in guttate psoriasis compared to plaque psoriasis.
Methods: Skin biopsy specimens from patients with guttate psoriasis (n=12), patients with plaque psoriasis (n=12), and normal skin controls (n=5) were used in the study. One-half were fixed in formalin and embedded in paraffin, and the other half were snap frozen and stored. Antibodies to HSP60 and TCRγδ were applied immunohistochemically. An immunoreactivity intensity distribution index (IRIDI) of HSP was calculated to express the proportion of the immunoreactive cells as well as the staining intensity in different layers of the epidermis. And the expression of HSP60 was also analyzed by Western blot analysis. TCRγδ-positive cell counts were semiquantitatively evaluated in 3 consecutive X400 microscopic fields, which were divided into epidermis and dermis.
Results: The mean IRIDI scores for HSP60 expression of guttate psoriasis were moderately higher than those for normal skin in the suprabasal layer (p＜0.05), but not significantly different from normal in the other layers and plaque psoriasis. And results from Western blot analysis were similar to the mean total IRIDI scores for HSP60 expression, but there was not significant differentiation amongst the three groups. TCRγδ-positive cell counts in the lesions of guttate and plaque psoriasis were significantly different from normal skin (p＜0.05) and TCRγδ-positive cell counts for guttate psoriasis were higher compared to those for plaque psoriasis (p＜0.05). There was no significant correlation between HSP60 and TCRγδ (p＞0.05).
Conclusion: This study suggests that up-regulation of HSP60 expression in the suprabasal layer may support the association of HSP60 in the etiology of psoriasis. TCRγδ may be involved in the pathogenesis of psoriasis, especially guttate psoriasis rather than plaque psoriasis, even though the correlation of HSP60 and TCRγδ was not significant. The mechanism of how they act to promote induction and aggravation in psoriasis remains to be elucidated.

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