IL-17 contributes to the development of chronic rejection in a murine heart transplant model.

Abstract:

BACKGROUND:Although interleukin-17 (IL-17) has been reported to participate in the pathogenesis of infectious, autoimmune and allergic disorders, the precise role in allograft rejection remains uncertain. This study illustrates that IL-17 contributes to the pathogenesis of chronic allograft rejection. RESULT:Utilizing a murine heterotopic heart transplant model system, IL-17-deficient recipient mice had decreased allograft inflammatory cell recruitment, decreased IL-6, MCP-1, and KC production, and reduced graft coronary artery disease (GCAD). Intragraft gamma delta (gammadelta) T cells appear to be the predominant source of IL-17 production. CONCLUSION:Therefore, IL-17 neutralization may provide a potential target for novel therapeutic treatment for cardiac allograft rejection.

journal_name

J Clin Immunol

authors

Itoh S,Nakae S,Axtell RC,Velotta JB,Kimura N,Kajiwara N,Iwakura Y,Saito H,Adachi H,Steinman L,Robbins RC,Fischbein MP

doi

10.1007/s10875-009-9366-9

subject

Has Abstract

pub_date

2010-03-01 00:00:00

pages

235-40

issue

2

eissn

0271-9142

issn

1573-2592

journal_volume

30

pub_type

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