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“未授权”的自然杀伤细胞主导了巨细胞病毒感染的反应。

'Unlicensed' natural killer cells dominate the response to cytomegalovirus infection.

机构信息

Department of Microbiology and Immunology and the Cancer Research Institute, University of California, San Francisco, California, USA.

出版信息

Nat Immunol. 2010 Apr;11(4):321-7. doi: 10.1038/ni.1849. Epub 2010 Feb 28.

DOI:10.1038/ni.1849
PMID:20190757
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2842453/
Abstract

Natural killer (NK) cells expressing inhibitory receptors that bind to self major histocompatibility complex (MHC) class I are 'licensed', or rendered functionally more responsive to stimulation, whereas 'unlicensed' NK cells lacking receptors for self MHC class I are hyporesponsive. Here we show that contrary to the licensing hypothesis, unlicensed NK cells were the main mediators of NK cell-mediated control of mouse cytomegalovirus infection in vivo. Depletion of unlicensed NK cells impaired control of viral titers, but depletion of licensed NK cells did not. The transfer of unlicensed NK cells was more protective than was the transfer of licensed NK cells. Signaling by the tyrosine phosphatase SHP-1 limited the proliferation of licensed NK cells but not that of unlicensed NK cells during infection. Thus, unlicensed NK cells are critical for protection against viral infection.

摘要

自然杀伤 (NK) 细胞表达的抑制性受体与自身主要组织相容性复合体 (MHC) Ⅰ类结合，被“许可”或使其对刺激更敏感，而缺乏自身 MHC Ⅰ类受体的“未许可”NK 细胞反应性较低。在这里，我们表明，与许可假说相反，未许可 NK 细胞是 NK 细胞介导的体内控制小鼠巨细胞病毒感染的主要介质。耗尽未许可的 NK 细胞会损害对病毒滴度的控制，但耗尽许可的 NK 细胞则不会。未许可 NK 细胞的转移比许可 NK 细胞的转移更具保护性。在感染过程中，酪氨酸磷酸酶 SHP-1 的信号转导限制了许可 NK 细胞的增殖，但不限制未许可 NK 细胞的增殖。因此，未许可的 NK 细胞对于抵抗病毒感染至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2e5/2842453/bcd730382e32/nihms176584f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2e5/2842453/1bcc68ac0d18/nihms176584f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2e5/2842453/5ca7f49747f1/nihms176584f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2e5/2842453/ed55cdbad541/nihms176584f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2e5/2842453/8dc82b4c6d62/nihms176584f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2e5/2842453/1e536b671033/nihms176584f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2e5/2842453/bcd730382e32/nihms176584f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2e5/2842453/1bcc68ac0d18/nihms176584f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2e5/2842453/5ca7f49747f1/nihms176584f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2e5/2842453/ed55cdbad541/nihms176584f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2e5/2842453/8dc82b4c6d62/nihms176584f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2e5/2842453/1e536b671033/nihms176584f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2e5/2842453/bcd730382e32/nihms176584f6.jpg

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[5]
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[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
NK cell responsiveness is tuned commensurate with the number of inhibitory receptors for self-MHC class I: the rheostat model.

J Immunol. 2009-4-15

[2]
Ly49H signaling through DAP10 is essential for optimal natural killer cell responses to mouse cytomegalovirus infection.

J Exp Med. 2009-4-13

[3]
Ly49P recognition of cytomegalovirus-infected cells expressing H2-Dk and CMV-encoded m04 correlates with the NK cell antiviral response.

J Exp Med. 2009-3-16

[4]
Breaking tolerance to self, circulating natural killer cells expressing inhibitory KIR for non-self HLA exhibit effector function after T cell-depleted allogeneic hematopoietic cell transplantation.

Blood. 2009-4-16

[5]
Adaptive immune features of natural killer cells.

Nature. 2009-1-29

[6]
Ly49D engagement on T lymphocytes induces TCR-independent activation and CD8 effector functions that control tumor growth.

J Immunol. 2009-1-1

[7]
Cutting edge: viral infection breaks NK cell tolerance to "missing self".

J Immunol. 2008-12-1

[8]
The strength of inhibitory input during education quantitatively tunes the functional responsiveness of individual natural killer cells.

Blood. 2009-3-12

[9]
Inhibitory receptor signaling via tyrosine phosphorylation of the adaptor Crk.

Immunity. 2008-10-17

[10]
Negative signaling by inhibitory receptors: the NK cell paradigm.

Immunol Rev. 2008-8

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