1994 Fiscal Year Final Research Report Summary
A STUDY FOR HUMAN INTERLEUKIN BETA PRODUCTION AND PROCESSING SYSTEM
| Project/Area Number |
04670638
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Dermatology
|
|---|
| Research Institution | MIE UNIVERSITY |
|---|
Principal Investigator |
MIZUTANI Hitoshi MIE UNIVERSITY,UNIVERSITY HOSPITAL,LECTURER, 医学部・付属病院, 講師 (30115737)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
INACHI Shin MIE UNIVERSITY,UNIVERSITY HOSPITAL,ASSISTANT, 医学部・付属病院, 助手 (60242939)
HASHIMOTO Kenji MIE UNIVERSITY,FACULTY OF MEDICINE,ASSISTANT, 医学部, 助手 (20252364)
|
|---|
| Project Period (FY) |
1992 – 1994
|
| Keywords | INTERLEUKIN-1 / CONVERTASE / RECEPTOR / PSORIASIS / PROCESSING / ANTAGONIST |
|---|
| Research Abstract |
We investigated epidermal IL-1 and IL-1 receptor system immunohistochemically and biochemically. Pro or mature form IL-1 beta specific antibody detected proIL-1 beta but not mature IL-1 beta in normal epidermis. Psoriatic epidermis decreased but contained hematopoietic cell derived mature IL-1 beta. These hematopoietic cells but nit keratinocyte contained IL-1 beta converting enzyme. Epidermis express signal transducable IL-1 receptor type 1 and non-signal transducable IL-1 receptor type 2 scarcely. Organ cultured normal skin and psoriatic lesional epidermis up-regulated expression of decoy IL-1 receptors : type 2 receptors but not type 1 receptors. The IL-1 receptor antagonist normally expressed on epedermis was exhausted in psoriatic lesions. The IL-1 expression was augmented in the inflammatory skin diseases but the over-expression of IL-1s were also strictly controlled multiple natural antagonistic systems : receptor antagonist and decoy receptor over expression.
|
