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Blood, 1 April 2008, Vol. 111, No. 7, pp. 3615-3625. Prepublished online as a Blood First Edition Paper on January 25, 2008; DOI 10.1182/blood-2007-09-111179. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2007-09-111179v1 111/7/3615    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Tian, L. Articles by Gahmberg, C. G. Search for Related Content PubMed PubMed Citation Articles by Tian, L. Articles by Gahmberg, C. G. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Shedded neuronal ICAM-5 suppresses T-cell activation Li Tian1, Jani Lappalainen2, Matti Autero1, Satu Hänninen1, Heikki Rauvala3, and Carl G. Gahmberg1 1 Division of Biochemistry, Department of Biologic and Environmental Sciences, Faculty of Biosciences, University of Helsinki, Helsinki; 2 Wihuri Research Institute, Helsinki; and 3 Neuroscience Center, University of Helsinki, Helsinki, Finland Intercellular adhesion molecules (ICAMs) bind to leukocyte β2 integrins, which, among other functions, provide costimulatory signals for T-cell activation. ICAM-5 (telencephalin) is expressed in the somadendritic region of neurons of the mammalian brain. The receptor for ICAM-5 is the integrin LFA-1, a major leukocyte integ-rin expressed in lymphocytes and microglia. In conditions of brain ischemia, epilepsy, and encephalitis, the soluble form of ICAM-5 (sICAM-5) has been detected in physiologic fluids. Here, we report that sICAM-5 attenuates the T-cell receptor-mediated activation of T cells as demonstrated by the decreased expression of the activation markers CD69, CD40L, and CD25 (IL-2R). This effect is most clearly seen in CD45ROLow (naive), and not in CD45ROHigh (memory) T cells, and is most effective early in priming, but not in the presence of strong costimulatory signals. Furthermore, sICAM-5 promotes the mRNA expression of the cytokines TGF-β1 and IFN-, but not TNF. The formation of sICAM-5 is promoted by activated T cells through the cleavage of ICAM-5 from neurons. This suggests that ICAM-5 is involved in immune privilege of the brain and acts as an anti-inflammatory agent. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. Huizinga, R. Q. Hintzen, K. Assink, M. van Meurs, and S. Amor T-cell responses to neurofilament light protein are part of the normal immune repertoire Int. Immunol., April 1, 2009; 21(4): 433 - 441. [Abstract] [Full Text] [PDF] X. Wu, Q. Liu, and R. Jiang Align human interactome with phenome to identify causative genes and networks underlying disease families Bioinformatics, January 1, 2009; 25(1): 98 - 104. [Abstract] [Full Text] [PDF]

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