한빛사 논문
Dong Sun Oha,b and Heung Kyu Leea,b,c*
aGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Republic of Korea
bBiomedical Science and Engineering Interdisciplinary Program, KAIST, Daejeon 34141, Republic of Korea
cKAIST Institute for Health Science and Technology, KAIST, Daejeon 34141, Republic of Korea
*Corresponding author
Abstract
Macroautophagy/autophagy has been implicated in cytoplasmic and viral antigen presentation on major histocompatibility complex (MHC) class II molecules. However, the role of autophagy in the presentation of phagocytized tumor-associated antigens in vivo remains unclear. Following the administration of apoptotic tumor cells and in vivo chemotherapy, mice with a dendritic cell–specific deletion of Atg5, a key autophagy gene, exhibit reduced CD4+ T-cell priming but not CD8+ cytotoxic T-cell priming. Interestingly, Atg5-deficient dendritic cells have an elevated expression of scavenger receptor CD36 and show excessive lipid accumulation. Atg5-deficient dendritic cells increased CD36-dependent phagocytosis of apoptotic tumor cells. CD36 blockade ameliorates elevated phagocytosis and increases CD4+ T-cell priming in dendritic cells; intratumoral CD36 blockade inhibits tumor growth. Our results demonstrate that Atg5 is required for proper antigen phagocytosis and presentation to MHC class II via modulation of CD36 in dendritic cells and may be a future therapeutic target for anti-tumor therapy.
Keywords: anti-tumor therapy, antigen presentation, ATG5, autophagy, CD36, dendritic cell, scavenger receptor
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