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Transplantation. 2010 May 27;89(10):1189-97. doi: 10.1097/TP.0b013e3181d720af.

IL-33 prolongs murine cardiac allograft survival through induction of TH2-type immune deviation.

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1
Department of Microbiology and Immunology, Guangdong Pharmaceutical University, Guangzhou, China.

Abstract

BACKGROUND:

In Th (T helper) 1/Th2 balance in response to signals given during donor antigen presentation, induction of allograft prolongation is more often related to Th2-type than with Th1-type immunity. Here, we examined the effect of interleukin (IL)-33, a novel member of the IL-1 family, on cardiac allograft survival in mice.

METHODS:

Mice heterotopic cardiac transplants were performed with sequential recipient sacrifice at anticipated time points to examine the immunoregulatory action of IL-33 in recipient mice.

RESULTS:

In vitro Th1-polarized CD4 T cells did not express ST2L; however, most CD4 T cells became ST2L on repeated stimulation under Th2-polarizing conditions. Similarly, we found that IL-33 was able to enhance the expression of Th2-associated cytokines (IL-5 and IL-13) but not interferon (IFN)-gamma. Treatment of recipient mice with IL-33 results in the improvement of allograft survival (more than 20 days) when compared with phosphate-buffered saline- or glutathione S-transferase-treated groups (all less than 9 days). Intracellular cytokine staining in CD4 splenocytes confirmed an increase in the percentage of IL-4 cells and a decrease in the percentage of IFN-gamma cells in IL-33 treated mice. In addition, IL-33 significantly enhanced the gene expression of Th2-type cytokines IL-4 and IL-5 but suppressed the Th1-type cytokine IFN-gamma mRNA levels in both allograft and recipient spleen.

CONCLUSION:

These data demonstrate that IL-33 serves as a potent inducer of Th2 immune response and can markedly contribute to the prolongation of cardiac allograft survival.

PMID:
20220570
DOI:
10.1097/TP.0b013e3181d720af
[Indexed for MEDLINE]
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