期刊
SCIENCE
卷 362, 期 6415, 页码 694-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aat5030
关键词
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资金
- NIH [U19-AI109725, T32 AI007163-40, F30DK108498]
- NCI [T32 CA 009621, 5R01 CA 190700, P30 CA 091842, 5R01 CA 193318]
- NIAID [U19-AI109948]
- NSF [DGE-1143954]
- Howard Hughes Medical Institute
- JAX KOMP program [U42OD011185]
- NATIONAL CANCER INSTITUTE [R01CA190700, P30CA091842, T32CA009621, R01CA193318] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [T32AI007163, U19AI109725, U19AI109948] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [F30DK108498, P30DK020579] Funding Source: NIH RePORTER
During the process of cross-presentation, viral or tumor-derived antigens are presented to CD8(+) T cells by Batf3-dependent CD8 alpha(+)/XCR1(+) classical dendritic cells (cDC1s). We designed a functional CRISPR screen for previously unknown regulators of cross-presentation, and identified the BEACH domain-containing protein WDFY4 as essential for cross-presentation of cell-associated antigens by cDC1s in mice. However, WDFY4 was not required for major histocompatibility complex class II presentation, nor for cross-presentation by monocyte-derived dendritic cells. In contrast to Batf3(-/-) mice, Wdfy4(-/-) mice displayed normal lymphoid and nonlymphoid cDC1 populations that produce interleukin-12 and protect against Toxoplasma gondii infection. However, similar to Batf3(-/-) mice, Wdfy4(-/-) mice failed to prime virus-specific CD8(+) T cells in vivo or induce tumor rejection, revealing a critical role for cross-presentation in antiviral and antitumor immunity.
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