Mechanisms of corneal endothelial cell inhibition of il-2 production

Pgi Mi, Hidetoshii Kawashima, Dale S Gregerson

Research output: Contribution to journalArticlepeer-review

Abstract

It has long been thought that certain types of cells in the eye may have immunoregulatory functions that provide its immune privilege. We have reported that CE cells can inhibit in vitro T cell proliferation and IL-2 production in response to antigen plus APC. The inhibition is neither MHC restricted nor species specific. CE cells do not inhibit IL-2 receptor expression or T cell response to exogenous IL-2. Here we report that CE cells inhibit IL-2 production of mouse KZO T cell hybridoma stimulated by antigen and APC, but not by PMA plus lonomycin which bypass the T cell receptor, CE cells do not block IL-2 gene transcription activated by PMA plus lonomycin, but block IL-2 gene transcription activated by antigen plus APC. Solid phase anti-CD3 mAb alone can stimulate KZO cells to make IL- 2, which is also inhibited by CE cells. CTLA4-Ig, which can block CD28 mediated costimulatory signaling pathway, does not block IL -2 production by KZO cells stimulated by antigen plus APC. These results show that KZO cells can make IL-2 independent of CD28 mediated signaling pathway so that CE cell inhibition is probably not due to a block of costimulation. Anti- phosphotyrosine Western Blot shows that CE cells induce tyrosine phosphorylation of two proteins approximately 100,000 Mr and 60,000 Mr in KZO cells. The properties of these are currently under investigation. This work is suppported by NIHEY09207 and RPB,Inc.

Original languageEnglish (US)
JournalFASEB Journal
Volume10
Issue number6
StatePublished - Dec 1 1996

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