April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
The Role of Allergic Conjunctivitis in the Exacerbation of Corneal Allograft Rejection
Author Affiliations & Notes
  • Nancy J. Reyes
    Ophthalmology, UT Southwestern Medical Center at Dallas, Dallas, Texas
  • Peter W. Chen
    Ophthalmology, Univ Texas Southwestern Medical Center, Dallas, Texas
  • Jerry Y. Niederkorn
    Ophthalmology, Univ Texas Southwestern Med Ctr, Dallas, Texas
  • Footnotes
    Commercial Relationships  Nancy J. Reyes, None; Peter W. Chen, None; Jerry Y. Niederkorn, None
  • Footnotes
    Support  National Institute of Health grants EY0007641 and EY016664 and an unrestricted grant from Research to Prevent Blindness
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 1141. doi:
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    • Get Citation

      Nancy J. Reyes, Peter W. Chen, Jerry Y. Niederkorn; The Role of Allergic Conjunctivitis in the Exacerbation of Corneal Allograft Rejection. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1141.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : This study focused on dissecting how allergic conjunctivitis (AC) abolishes immune privilege and exacerbates corneal allograft rejection.

Methods: : AC was induced in BALB/c mice by intraperitoneal immunization with short ragweed (SRW) pollen and daily topical challenge with SRW pollen. Mice were given orthotopic C57BL/6 (B6) corneal allografts. Allospecific T cell responses were evaluated using a mixed lymphocyte reaction (MLR) with B6 alloantigens as stimulators and BALB/c CD4+ T cells from mice that had AC and had rejected their corneal allografts (allergic rejectors) or normal rejectors as responders. Proliferation of CD4+ T cells was assessed by thymidine incorporation. Development of allospecific cytotoxic T lymphocyte (CTL) responses was evaluated in a conventional 51Cr-release assay. T regulatory cells (Tregs) were evaluated by isolating CD4+CD25+ Tregs from BALB/c hosts with clear corneal allografts at day 21 and co-culturing them with anti-CD3-stimulated CD4+ T cells from naïve mice, mice with AC, or IL-4R-/- mice in the absence or presence of recombinant IL-4 (rIL-4). Treg-mediated suppression of CD4+ T cell proliferation was measured by thymidine incorporation.

Results: : CD4+ T cells from allergic rejectors did not display enhanced proliferation to B6 alloantigens. Allergic rejectors, like normal rejectors, did not generate CTLs. Suppression assays showed that Tregs isolated from corneal allograft acceptor mice suppressed the proliferation of activated CD4+ effector T cells. Treg-mediated suppression was lost in the presence of rIL-4. Tregs were unable to suppress proliferation of effector T cells from mice with AC even in the absence of rIL-4. However, Tregs were able to suppress proliferation of IL-4R-/- effector T cells, even in the presence of rIL-4, thereby confirming that IL-4 rendered the immune effector cells to become resistant to suppression by Tregs.

Conclusions: : AC does not abrogate the immune privilege of corneal allografts by promoting quantitative or qualitative changes in T cell-mediated alloimmune responses, but appears to alter corneal allograft-induced Tregs. Th2 cytokines, namely IL-4, generated during AC render effector T cells resistant to Treg suppression. Future investigations will evaluate how the effect of IL-4 can be blocked to increase corneal allograft survival in hosts with allergic diseases.

Keywords: conjunctivitis • cornea: basic science • immune tolerance/privilege 

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