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1994 Fiscal Year Final Research Report Summary

Immunological Studies On The Mechanisms Of Experimental Autoimmune Dacryoadenitis

Research Project

Project/Area Number 05671453
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field Ophthalmology
Research InstitutionHOKKAIDO UNIVERSITY

Principal Investigator

TAGAWA Yoshitsugu  Hokkaido University School of Medicine, Associate Professor, 医学部, 助教授 (40109426)

Project Period (FY) 1993 – 1994
KeywordsAutoimmune dacryoadenitis / Experimental model / Sell-Mediated Immunity / Helper T cell
Research Abstract

It has been reported that a soluble lacrimal gland antigen (LG-Ag) was capable of inducing experimental autoimmune dacryoadenitis (EAD) in SJL/J mice. (S.H.Liu, et al, Invest.Ophthalmol Vis Sci, 33 : 2029.1992) This animal model is thought to be a good model in the study of dry eye syndrome including Sjogren syndrome. In this study we analyzed the lymphocyte subsets of infiltrating cells, especially T cells, in the lacrimal gland of EAD.
We immunized ten female SJL/J mice with LG-Ag (100mug) in complete Freund's adjuvant (CFA). Thirty and fourty days after immunization, the exorbital lacrimal glands were removed and fixed in liquid nitrogen. Five micron cryostat sections were stained by ABC technique of immunoperoxidase methods. The following monoclonal antibodies were used : 1) anti-Thy-1,2) anti-L3T4,3) anti-Lyt-2.
Histologically many mononuclear inflammatory cells were observed mainly around the lacrimal ducts with considerable destruction of LG acini and ducts. Immunohistochemically many Thy-1 positive lymphocytes were seen in the area or infiltrating cells. L3T4 of helper T cells seemed to be a predominant population of T cells whereas Lyt-2 of suppressor/cytotoxic T cells were a minor population of T cells.
The above findings indicate that T cells, especially helper T cells, may play a role in the immunopathology of EAD.

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Published: 1999-03-16  

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