A key role for ICAM-I in generating effector cells mediating inflammatory responses
AuthorCamacho, SA; Heath, WR; Carbone, FR; Sarvetnick, N; LeBon, A; Karlsson, L; Peterson, PA; Webb, SR
Source TitleNATURE IMMUNOLOGY
PublisherNATURE PUBLISHING GROUP
AffiliationMicrobiology And Immunology
Document TypeJournal Article
CitationsCamacho, S. A., Heath, W. R., Carbone, F. R., Sarvetnick, N., LeBon, A., Karlsson, L., Peterson, P. A. & Webb, S. R. (2001). A key role for ICAM-I in generating effector cells mediating inflammatory responses. NATURE IMMUNOLOGY, 2 (6), pp.523-529. https://doi.org/10.1038/88720.
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C1 - Journal Articles Refereed
We investigated how the accessory molecule interactions encountered during T cell priming influence T cell-mediated destruction of insulin-producing beta cells and lead to type 1 diabetes. T cell receptor (TCR)-transgenic CD4+ T cells were primed under controlled conditions in vitro before being adoptively transferred into transgenic recipients expressing membrane ovalbumin under the control of the rat insulin promoter (RIP-mOVA). During priming, antigen-presenting cell expression of B7-1 without intracellular adhesion molecule 1 (ICAM-1) led to the generation of effector cells that migrated to the pancreata of RIP-mOVA recipients but did not cause diabetes. In contrast, when T cells were primed with APCs expressing both B7-1 and ICAM-1, pronounced destruction of beta cells and a rapid onset of diabetes were observed. Pathogenicity was associated with T cell production of the macrophage-attracting chemokines CCL3 and CCL4. Thus, interactions of lymphocyte function-associated antigen 1 with ICAM-1 during priming induce both qualitative and quantitative alterations in T effector function and induce potentially autodestructive responses.
KeywordsCellular Immunology; Immune System and Allergy
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