Exogenous recombinant interleukin-2 abrogates anterior-chamber-associated immune deviation

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

Alloantigens placed into the anterior chamber of the eye elicit antigen-specific suppression of systemic de-layed-type hypersensitivity (DTH) responses and severe impairment of skin allograft rejection. This pattern of immunological impairment has been termed anterior-chamber-associated immune deviation (ACAID). We have previously proposed that ACAID is the underlying mechanism responsible for immunologic privilege within the anterior chamber of the eye. The present study examined the role of interleukin 2 (IL-2) in the induction of ACAID. As previously shown, intracameral inoculation of P815 cells into allogeneic BALB/c recipients resulted in antigen specific suppression of DTH responses. However, subcutaneous administration of recombinant IL-2 along with intracameral inoculation of P815 cells prevented ACAID and permitted the development of positive DTH responsiveness in BALB/c hosts. In order to abrogate ACAID, exogenous IL-2 was required only during the first 72 hr following anterior chamber presentation of alloantigens. Collectively, the results indicate that induction of ACAID and the antigen-specific suppression of systemic DTH responses are due to IL-2 deficiency during the early stages of antigen perception. This in turn implies that the immunological privilege within the anterior chamber of the eye may pivot on the deficiency of a single lymphokine, interleukin 2.

Original languageEnglish (US)
Pages (from-to)523-528
Number of pages6
JournalTransplantation
Volume43
Issue number4
DOIs
StatePublished - Apr 1987

ASJC Scopus subject areas

  • Transplantation

Fingerprint Dive into the research topics of 'Exogenous recombinant interleukin-2 abrogates anterior-chamber-associated immune deviation'. Together they form a unique fingerprint.

  • Cite this