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中华危重症医学杂志(电子版) ›› 2022, Vol. 15 ›› Issue (04) : 332 -336. doi: 10.3877/cma.j.issn.1674-6880.2022.04.015

综述

固有淋巴细胞的动员与迁移在脓毒症中的作用及机制
叶璟1, 赖登明2, 舒强3,()   
  1. 1. 310052 杭州,浙江大学医学院附属儿童医院 国家儿童健康与疾病临床医学研究中心SICU
    2. 310052 杭州,浙江大学医学院附属儿童医院 国家儿童健康与疾病临床医学研究中心新生儿外科
    3. 310052 杭州,浙江大学医学院附属儿童医院 国家儿童健康与疾病临床医学研究中心心胸外科
  • 收稿日期:2021-11-02 出版日期:2022-08-31
  • 通信作者: 舒强
  • 基金资助:
    国家自然科学基金项目(81901989)
  • Received:2021-11-02 Published:2022-08-31
引用本文:

叶璟, 赖登明, 舒强. 固有淋巴细胞的动员与迁移在脓毒症中的作用及机制[J]. 中华危重症医学杂志(电子版), 2022, 15(04): 332-336.

固有淋巴细胞(innate lymphoid cells,ILCs)是近年受到广泛关注的细胞的免疫效应细胞类型[1]。这些细胞源自淋巴样前体,是脓毒症早期抵抗外界病原体感染的第一道防线[2],尽管缺少特异性/泛特异性抗原受体,其活化不依赖于对抗原的识别,但这些细胞仍显示出广泛的效应功能。它们可以通过病原体识别受体的表达快速响应病原体或受损组织的信号,或对两者均产生反应,从而导致多种细胞因子的分泌,影响在感染/损伤部位产生的免疫反应类型[3]。过度、持续的创伤应激可导致固有免疫反应失衡,诱发创伤后免疫麻痹,这是严重多发伤后脓毒症和多器官功能障碍综合征高发的主要诱因之一[4]。与适应性免疫应答相比,ILCs可能可以对某些病原体提供更快的反应,并且在调节随后的固有和适应性免疫反应中发挥作用,是跨越固有和适应性免疫系统之间的桥梁[5]

1
Artis D, Spits H. The biology of innate lymphoid cells[J]. Nature, 2015, 517 (7534): 293-301.
2
Sonnenberg GF, Artis D. Innate lymphoid cells in the initiation, regulation and resolution of inflammation[J]. Nat Med, 2015, 21 (7): 698-708.
3
Klose CS, Artis D. Innate lymphoid cells as regulators of immunity, inflammation and tissue homeostasis[J]. Nat Immunol, 2016, 17 (7): 765-774.
4
李镇文,杨想平,唐朝晖.固有免疫反应在严重多发伤后机体免疫麻痹中的核心作用[J/CD].中华危重症医学杂志(电子版)202114(3):248-251.
5
Eberl G, Colonna M, Di Santo JP, et al. Innate lymphoid cells. Innate lymphoid cells: a new paradigm in immunology[J]. Science, 2015, 348 (6237): aaa6566.
6
Vivier E, Artis D, Colonna M, et al. Innate lymphoid cells: 10 years on[J]. Cell, 2018, 174 (5): 1054-1066.
7
Montaldo E, Vacca P, Vitale C, et al. Human innate lymphoid cells[J]. Immunol Lett, 2016 (179): 2-8.
8
Constantinides MG, McDonald BD, Verhoef PA, et al. A committed precursor to innate lymphoid cells[J]. Nature, 2014, 508 (7496): 397-401.
9
Klose CSN, Flach M, Mohle L, et al. Differentiation of type 1 ILCs from a common progenitor to all helper-like innate lymphoid cell lineages[J]. Cell, 2014, 157 (2): 340-356.
10
Zhong C, Zheng M, Cui K, et al. Differential expression of the transcription factor GATA3 specifies lineage and functions of innate lymphoid cells[J]. Immunity, 2020, 52 (1): 83-95.e4.
11
Moretta F, Petronelli F, Lucarelli B, et al. The generation of human innate lymphoid cells is influenced by the source of hematopoietic stem cells and by the use of G-CSF[J]. Eur J Immunol, 2016, 46 (5): 1271-1278.
12
Munneke JM, Bjorklund AT, Mjosberg JM, et al. Activated innate lymphoid cells are associated with a reduced susceptibility to graft-versus-host disease[J]. Blood, 2014, 124 (5): 812-821.
13
Lim AI, Li Y, Lopez-Lastra S, et al. Systemic human ILC precursors provide a substrate for tissue ILC differentiation[J]. Cell, 2017, 168 (6): 1086-1100.e10.
14
Zhao T, Li Y, Liu B, et al. Inhibition of histone deacetylase 6 restores innate immune cells in the bone marrow in a lethal septic model[J]. J Trauma Acute Care Surg, 2016, 80 (1): 34-40; discussion 40-41.
15
Mueller SN, Mackay LK. Tissue-resident memory T cells: local specialists in immune defence[J]. Nat Rev Immunol, 2016, 16 (2): 79-89.
16
Moro K, Kabata H, Tanabe M, et al. Interferon and IL-27 antagonize the function of group 2 innate lymphoid cells and type 2 innate immune responses[J]. Nat Immunol, 2016, 17 (1): 76-86.
17
Monticelli LA, Sonnenberg GF, Abt MC, et al. Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus[J]. Nat Immunol, 2011, 12 (11): 1045-1054.
18
Abt MC, Lewis BB, Caballero S, et al. Innate immune defenses mediated by two ILC subsets are critical for protection against acute clostridium difficile infection[J]. Cell Host Microbe, 2015, 18 (1): 27-37.
19
Quatrini L, Wieduwild E, Guia S, et al. Host resistance to endotoxic shock requires the neuroendocrine regulation of group 1 innate lymphoid cells[J]. J Exp Med, 2017, 214 (12): 3531-3541.
20
Griffith JW, Sokol CL, Luster AD. Chemokines and chemokine receptors: positioning cells for host defense and immunity[J]. Annu Rev Immunol, 2014 (32): 659-702.
21
Stehle C, Rückert T, Fiancette R, et al. T-bet and RORα control lymph node formation by regulating embryonic innate lymphoid cell differentiation[J]. Nat Immunol, 2021, 22 (10): 1231-1244.
22
O'Sullivan TE, Rapp M, Fan X, et al. Adipose-resident group 1 innate lymphoid cells promote obesity-associated insulin resistance[J]. Immunity, 2016, 45 (2): 428-441.
23
Gasteiger G, Fan X, Dikiy S, et al. Tissue residency of innate lymphoid cells in lymphoid and nonlymphoid organs[J]. Science, 2015, 350 (6263): 981-985.
24
Zhu J. T helper 2 (Th2) cell differentiation, type 2 innate lymphoid cell (ILC2) development and regulation of interleukin-4 (IL-4) and IL-13 production[J]. Cytokine, 2015, 75 (1): 14-24.
25
吴瑶,祝筱梅,郭方,等. Ⅱ型固有淋巴细胞在炎症性疾病中的作用及意义[J].中华急诊医学杂志202130(7):907-911.
26
Liew FY, Girard JP, Turnquist HR. Interleukin-33 in health and disease[J]. Nat Rev Immunol, 2016, 16 (11): 676-689.
27
Bessa J, Meyer CA, de Vera Mudry MC, et al. Altered subcellular localization of IL-33 leads to non-resolving lethal inflammation[J]. J Autoimmun, 2014 (55): 33-41.
28
Stier MT, Zhang J, Goleniewska K, et al. IL-33 promotes the egress of group 2 innate lymphoid cells from the bone marrow[J]. J Exp Med, 2018, 215 (1): 263-281.
29
Chun TT, Chung CS, Fallon EA, et al. Group 2 innate lymphoid cells (ILC2s) are key mediators of the inflammatory response in polymicrobial sepsis[J]. Am J Pathol, 2018, 188 (9): 2097-2108.
30
Lai D, Tang J, Chen L, et al. Group 2 innate lymphoid cells protect lung endothelial cells from pyroptosis in sepsis[J]. Cell Death Dis, 2018, 9 (3): 369.
31
Ito I, Bhopale KK, Kobayashi M, et al. Lamina propria group 2 innate lymphoid cells impair the antibacterial defense of burned mice to enterococcal translocation[J]. J Leukoc Biol, 2017, 102 (6): 1451-1460.
32
Chen W, Lai D, Li Y, et al. Neuronal-activated ILC2s promote IL-17A production in lung γδ T cells during sepsis[J]. Front Immunol, 2021 (12): 670676
33
Bruchard M, Geindreau M, Perrichet A, et al. Recruitment and activation of type 3 innate lymphoid cells promote antitumor immune responses[J]. Nat Immunol, 2022, 23 (2): 262-274.
34
Rankin LC, Girard-Madoux MJ, Seillet C, et al. Complementarity and redundancy of IL-22-producing innate lymphoid cells[J]. Nat Immunol, 2016, 17 (2): 179-186.
35
Lim AI, Di Santo JP. ILC-poiesis: ensuring tissue ILC differentiation at the right place and time[J]. Eur J Immunol, 2019, 49 (1): 11-18.
36
Hepworth MR, Monticelli LA, Fung TC, et al. Innate lymphoid cells regulate CD4+ T-cell responses to intestinal commensal bacteria[J]. Nature, 2013, 498 (7452): 113-117.
37
Mortha A, Chudnovskiy A, Hashimoto D, et al. Microbiota-dependent crosstalk between macrophages and ILC3 promotes intestinal homeostasis[J]. Science, 2014, 343 (6178): 1249288.
38
Carvelli J, Piperoglou C, Bourenne J, et al. Imbalance of circulating innate lymphoid cell subpopulations in patients with septic shock[J]. Front Immunol, 2019 (10): 2179.
39
Lim AI, Verrier T, Vosshenrich CA, et al. Developmental options and functional plasticity of innate lymphoid cells[J]. Curr Opin Immunol, 2017 (44): 61-68.
40
Souza-Fonseca-Guimaraes F, Parlato M, Philippart F, et al. Toll-like receptors expression and interferon-γ production by NK cells in human sepsis[J]. Crit Care, 2012, 16 (5): R206.
41
Guo Y, Patil NK, Luan L, et al. The biology of natural killer cells during sepsis[J]. Immunology, 2018, 153 (2): 190-202.
42
Hiraki S, Ono S, Kinoshita M, et al. Neutralization of IL-10 restores the downregulation of IL-18 receptor on natural killer cells and interferon-γ production in septic mice, thus leading to an improved survival[J]. Shock, 2012, 37 (2): 177-182.
43
陈敏,袁佳辉,郭冬阳,等. CXC趋化因子配体12/CXC趋化因子受体4轴在脓毒症中的研究进展[J/CD].中华危重症医学杂志(电子版)202012(3):225-228.
44
Pastille E, Pohlmann S, Wirsdorfer F, et al. A disturbed interaction with accessory cells upon opportunistic infection with Pseudomonas aeruginosa contributes to an impaired IFN-gamma production of NK cells in the lung during sepsis-induced immunosuppression[J]. Innate Immun, 2015, 21 (2): 115-126.
45
Zang J, Ye J, Zhang C, et al. Senescent hepatocytes enhance natural killer cell activity via the CXCL-10/CXCR3 axis[J]. Exp Ther Med, 2019, 18 (5): 3845-3852.
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