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Blood, 15 May 2007, Vol. 109, No. 10, pp. 4320-4327. Prepublished online as a Blood First Edition Paper on February 6, 2007; DOI 10.1182/blood-2006-11-053769. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2006-11-053769v1 109/10/4320    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 Chung, J.-S. Articles by Ariizumi, K. Search for Related Content PubMed PubMed Citation Articles by Chung, J.-S. Articles by Ariizumi, K. Related Collections Immunobiology Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY DC-HIL is a negative regulator of T lymphocyte activation Jin-Sung Chung1, Kota Sato1, Irene I. Dougherty1, Ponciano D. Cruz, Jr1, and Kiyoshi Ariizumi1 1 Department of Dermatology, The University of Texas Southwestern Medical Center and Dermatology Section (Medical Service), Dallas Veterans Affairs Medical Center, Dallas, TX T-cell activation is the net product of competing positive and negative signals transduced by regulatory molecules on antigen-presenting cells (APCs) binding to corresponding ligands on T cells. Having previously identified DC-HIL as a receptor expressed by APCs that contains an extracellular immunoglobulin (Ig)–like domain, we postulated that it plays a role in T-cell activation. To probe this function, we created soluble recombinant DC-HIL, which we observed to bind activated (but not resting) T cells, indicating that expression of the putative ligand on T cells is induced by activation. Binding of DC-HIL to naive T cells attenuated these cells' primary response to anti-CD3 antibody, curtailing IL-2 production, and preventing entry into the cell cycle. DC-HIL also inhibited reactivation of T cells previously activated by APCs (secondary response). By contrast, addition of soluble DC-HIL to either allogeneic or ovalbumin-specific lymphocyte reactions augmented T-cell proliferation, and its injection into mice during the elicitation (but not sensitization) phase of contact hypersensitivity exacerbated ear-swelling responses. Mutant analyses showed the inhibitory function of DC-HIL to reside in its extracellular Ig-like domain. We conclude that endogenous DC-HIL is a negative regulator of T lymphocyte activation, and that this native inhibitory function can be blocked by exogenous DC-HIL, leading to enhanced immune responses. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J.-S. Chung, T. Yudate, M. Tomihari, H. Akiyoshi, P. D. Cruz Jr., and K. Ariizumi Binding of DC-HIL to Dermatophytic Fungi Induces Tyrosine Phosphorylation and Potentiates Antigen Presenting Cell Function J. Immunol., October 15, 2009; 183(8): 5190 - 5198. [Abstract] [Full Text] [PDF] J.-S. Chung, I. Dougherty, P. D. Cruz Jr., and K. Ariizumi Syndecan-4 Mediates the Coinhibitory Function of DC-HIL on T Cell Activation J. Immunol., November 1, 2007; 179(9): 5778 - 5784. [Abstract] [Full Text] [PDF]

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