HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Crotzer, V. L. Articles by Blum, J. S. Search for Related Content PubMed PubMed Citation Articles by Crotzer, V. L. Articles by Blum, J. S.

Autophagy and Its Role in MHC-Mediated Antigen Presentation¹

Department of Microbiology and Immunology and the Walther Oncology Center, Indiana University School of Medicine and the Walther Cancer Institute, Indianapolis, IN 46202

Intracellular degradation by autophagy plays a role in the maintenance of cellular homeostasis under normal conditions and during periods of cellular stress. Autophagy has also been implicated in several other cellular processes including immune recognition and responsiveness. More specifically, autophagy has been identified as a route by which cytoplasmic and nuclear Ag are delivered to MHC class II molecules for presentation to CD4⁺ T cells. Autophagy has also recently been implicated in MHC class I cross-presentation of tumor Ag and the activation of CD8⁺ T cells. This review discusses the role of autophagy in modulating MHC class I and class II Ag presentation as well as its implication in regulating autoimmunity and tolerance, tumor immunity, and host defense against intracellular pathogens.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ V.L.C. is supported by a Career Development Award from the Melanoma Research Foundation. National Institutes of Health AI49589 supported the effort of J.S.B.

² Address correspondence and reprint requests to Dr. Janice S. Blum, Medical Science Building Room 420, 635 Barnhill Drive, Indianapolis, Indiana, 46202-5120. E-mail address: jblum{at}iupui.edu

³ Abbreviations used in this paper: CMA, chaperone-mediated autophagy; ALIS, aggresome-like induced structures; Atg, autophagy-related gene; cTEC, cortical thymic epithelial cell; DC, dendritic cell; EBNA, EBV nuclear Ag; ER, endoplasmic reticulum; GAD, glutamic acid decarboxylase; hsc70, heat shock cognate 70-kDa protein; Ii, invariant chain; LAMP, lysosome-associated membrane protein; 3-MA, 3-methyladenine; MP1, influenza matrix protein 1; mTOR, mammalian target of rapamycin; siRNA, small interfering RNA.

This article has been cited by other articles:

				E. White and R. S. DiPaola The Double-Edged Sword of Autophagy Modulation in Cancer Clin. Cancer Res., September 1, 2009; 15(17): 5308 - 5316. [Abstract] [Full Text] [PDF]

				H. Matsui, M. Shibata, B. Brown, A. Labelle, C. Hegadorn, C. Andrews, M. Chuah, T. VandenDriessche, C. H. Miao, C. Hough, et al. A murine model for induction of long-term immunologic tolerance to factor VIII does not require persistent detectable levels of plasma factor VIII and involves contributions from Foxp3+ T regulatory cells Blood, July 16, 2009; 114(3): 677 - 685. [Abstract] [Full Text] [PDF]