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Absence of Allograft ICAM-1 Attenuates Alloantigen-Specific T Cell Priming, But Not Primed T Cell Trafficking into the Graft, to Mediate Acute Rejection¹

Qi-Wei Zhang^*, Danielle D. Kish^* and Robert L. Fairchild^2,*,,

^* Department of Immunology and Urological Institute, Cleveland Clinic Foundation, Cleveland, OH 44195; and Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106

The expression and function of ICAM-1 are critical components in the initiation and elicitation of many T cell-mediated responses. Whether ICAM-1 expression is required on the T cells or on the APC during T cell priming remains unclear. To address this issue in alloantigen-specific T cell activation, the priming and function of T cells in response to heart allografts from MHC-mismatched wild-type vs ICAM-1^-/- donors were tested. Wild-type C57BL/6 (H-2^b) heart allografts were rejected by A/J (H-2^a) recipients on days 7–9, whereas B6.ICAM-1^-/- allografts survived until days 18–23 post-transplant. On day 7 post-transplant, infiltrating macrophages and CD4⁺ and CD8⁺ T cells in the ICAM-1^-/- allografts were 20–30% those observed in the wild-type allografts. ELISPOT analyses indicated that the number of alloantigen-specific T cells producing IFN- from recipients of ICAM-1-deficient grafts was 60% lower than that from recipients of wild-type allografts. On day 16 post-transplant, these numbers did not markedly increase in ICAM-1-deficient allograft recipients. Consistent with the reduced priming of alloreactive T cells, isolated dendritic cells from ICAM-1^-/- mice stimulated allogeneic T cell proliferation poorly compared with wild-type dendritic cells. When A/J mice were primed with wild-type dendritic cells and then received wild-type or ICAM-1-deficient heart allografts 3 days later, the primed recipients rejected the wild-type and ICAM-1^-/- allografts on days 5–6 post-transplant. These results indicate that optimal priming of alloreactive T cells requires allograft expression of ICAM-1, but, once primed, recipient T cell infiltration into the allograft is independent of graft ICAM-1 expression.

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