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DOI10.1126/science.aax4040
PIRs mediate innate myeloid cell memory to nonself MHC molecules
Hehua Dai; Peixiang Lan; Daqiang Zhao; Khodor Abou-Daya; Wentao Liu; Wenhao Chen; Andrew J. Friday; Amanda L. Williams; Tao Sun; Jianjiao Chen; Wei Chen; Steven Mortin-Toth; Jayne S. Danska; Chris Wiebe; Peter Nickerson; Tengfang Li; Lisa R. Mathews; Hêth R. Turnquist; Matthew L. Nicotra; Sebastien Gingras; Eiji Takayama; Hiromi Kubagawa; Mark J. Shlomchik; Martin H. Oberbarnscheidt; Xian C. Li; Fadi G. Lakkis
2020-06-05
发表期刊Science
出版年2020
英文摘要Immunological memory is a phenomenon by which immune cells can quickly recognize an antigen that the host has previously encountered. Certain cells of the innate immune system exhibit memory-like responses know as trained immunity. Rapid, antigen-specific secondary (anamnestic) responses were long thought to be the domain of B and T cells. However, Dai et al. report that monocytes and macrophages can acquire memory specific for particular major histocompatibility complex I antigens using paired A-type immunoglobulin-like receptors (PIR-As) (see the Perspective by Dominguez-Andrés and Netea). This pathway contributes to recognition and rejection of allograft-transplanted tissue from a donor of the same species. Genetic depletion or blockade of PIR-As in mice diminished the rejection of kidney and heart allografts. This work, which expands immunological memory to include myeloid cells, points to targets that may improve organ transplantation outcomes in the future. Science , this issue p. [1122][1]; see also p. [1052][2] Immunological memory specific to previously encountered antigens is a cardinal feature of adaptive lymphoid cells. However, it is unknown whether innate myeloid cells retain memory of prior antigenic stimulation and respond to it more vigorously on subsequent encounters. In this work, we show that murine monocytes and macrophages acquire memory specific to major histocompatibility complex I (MHC-I) antigens, and we identify A-type paired immunoglobulin-like receptors (PIR-As) as the MHC-I receptors necessary for the memory response. We demonstrate that deleting PIR-A in the recipient or blocking PIR-A binding to donor MHC-I molecules blocks memory and attenuates kidney and heart allograft rejection. Thus, innate myeloid cells acquire alloantigen-specific memory that can be targeted to improve transplant outcomes. [1]: /lookup/doi/10.1126/science.aax4040 [2]: /lookup/doi/10.1126/science.abc2660
领域气候变化 ; 资源环境
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文献类型期刊论文
条目标识符http://119.78.100.173/C666/handle/2XK7JSWQ/273446
专题气候变化
资源环境科学
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Hehua Dai,Peixiang Lan,Daqiang Zhao,et al. PIRs mediate innate myeloid cell memory to nonself MHC molecules[J]. Science,2020.
APA Hehua Dai.,Peixiang Lan.,Daqiang Zhao.,Khodor Abou-Daya.,Wentao Liu.,...&Fadi G. Lakkis.(2020).PIRs mediate innate myeloid cell memory to nonself MHC molecules.Science.
MLA Hehua Dai,et al."PIRs mediate innate myeloid cell memory to nonself MHC molecules".Science (2020).
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