1990 Fiscal Year Final Research Report Summary
Studies on the Pathogenesis of Skin Lesions of Psoriasis and Related
Project/Area Number |
63480243
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Research Category |
Grant-in-Aid for General Scientific Research (B)
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Allocation Type | Single-year Grants |
Research Field |
Dermatology
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Research Institution | Tohoku University |
Principal Investigator |
TAGAMI Hachiro Sch. of Med, Dermatology Professor Dermatoses, 医学部, 教授 (60026911)
|
Co-Investigator(Kenkyū-buntansha) |
TAKEMATSU Hideaki Sch. of Med, Dermatology Assistant Professor, 医学部・附属病院, 講師 (80124600)
KATO Taizo Sch. of Med, Dermatology Associate Professor, 医学部, 助教授 (20004898)
|
Project Period (FY) |
1988 – 1990
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Keywords | cytokine / interleukin l / interleukin 8 / psoriasis / pustular psoriasis / pustulosis palmaris et plantaris / OK 432 / streptococcal antigen |
Research Abstract |
The autologous mixed lymphocyte reaction of the peripheral blood mononuclear cells (PBMs) of psoriatic patients was significantly lower than that of normal subjects or that of patients with atopic dermatitis. Moreover, Their reactivity to streptococcal preparation OK 432 was also greatly reduced as compared with those of normal subjects, although their reactivity to T cell growth factors such as IL-2, IL-3, IL-4, and GMCSF was not different from that of the controls. Similar comparison was made between patients with pustular psoriasis and those with pustulosis palmaris et plantaris. The PBMs of the former showed significantly decreased reactivity to the stimulus of OK 432 as compared to those of the latter. Thus, although the histopathologic features of these two pustular dermatoses are similar each other, there seem to be a difference between these two dermatoses. Studies of psoriatic scale extracts demonstrated a decrease in IL-l alpha and beta concentrations and the absence of TNF-alpha in contrast to GMCSF and INF-gamma which were found to be increased in the scale extracts. Human epidermal keratinocytes constitutively produce a neutrophil chemotacitc cytokine of 11 Kd that is distinct from IL-1 with their growth in vitro. Blocking study with anti-IL8 antiserum confirmed that this cytokine is IL-8. Its release form keratinocytes was stimulated by IL-1, TNF-alpha and LPS.
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