Anterior chamber–associated immune deviation and its impact on corneal allograft survival

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Purpose of review

Anterior chamber–associated immune deviation is a form of immune tolerance elicited by ocular antigens and corneal transplants. It produces antigen-specific downregulation of T-helper 1 immune responses and promotes corneal allograft survival. This review discusses recent insights in the induction of anterior chamber–associated immune deviation.

Recent findings

Although initial findings suggested that anterior chamber–associated immune deviation was a preferential activation of T-helper 2 immunity, recent findings indicate that T-helper 2 cytokines, such as interleukin-4 and interleukin-13, and T-helper 2 transcription factors are not needed. Findings indicate that ocular antigen-presenting cells migrate to the spleen and release antigenic peptides that are captured and reprocessed by splenic B cells, which present antigenic peptides to T cells on both major histocompatibility complex class I and class II molecules, leading to the generation of CD8+ T-regulatory cells and CD4+ T-regulatory cells.


Anterior chamber–associated immune deviation is a complex immunoregulatory phenomenon involving multiple cell populations and four organ systems. Anterior chamber–associated immune deviation reduces the risk for immune-mediated inflammation in the eye and promotes corneal allograft survival. Understanding the mechanisms may help improve the survival of other organ transplants that are at risk for immune rejection.

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