Progress on Siglecs in sepsis

doi:10.3877/cma.j.issn.1674-1358.2018.05.001

Abstract

Abstract:

Siglecs are cell surface transmenbrane receptor and are expressed on the immune cells, which regulated the immune balance in inflammation diseases. Sepsis is organ dysfunction induced by infection, the pathogenesis of sepsis contains the immune disorder, inflammatory reaction and coagulation dysregulation. In this article, we reviewed the role of Siglecs in the pathogenesis of sepsis was reviewed. Siglec-1, Siglec-5 and Siglec-14 play bidirectional role by regulating the inflammation and immunity. Siglec-2 modulates the immune balance in inflammation through regulating B cell and T cell response. Siglec-9 modulates macrophagepolarization and restrain the function of neutrophils during infection through the endocytosis of toll-like receptor 4 (TLR4). Siglec-10 inhibits the danger-associated molecular pattern (DAMP) and helps T cells initiate antigen-antibody responses, and reduces the number of B cells, thus reducing inflammation. Modulation of Siglecs function in different stages of sepsis have potential therapeutic significance in the treatment of sepsis.

Key words: Siglecs, Infection, Sepsis, Inflammation

Sasa Chu, Na You, Maorong Wang. Progress on Siglecs in sepsis[J]. Chinese Journal of Experimental and Clinical Infectious Diseases(Electronic Edition), 2018, 12(05): 417-421.

/ / Recommend

Add to citation manager EndNote|Ris|BibTeX

URL: https://zhsyhlcgrbzz.cma-cmc.com.cn/EN/10.3877/cma.j.issn.1674-1358.2018.05.001

https://zhsyhlcgrbzz.cma-cmc.com.cn/EN/Y2018/V12/I05/417

References 51

[10]	Wu Y, Lan C, Ren D, et al. Induction of siglec-1 by endotoxin tolerance suppresses the innate immune response by promoting TGF-β1 production[J]. J Biol Chem,2016,291(23):12370-12382.
[11]	Sewald X, Ladinsky MS, Uchil PD, et al. Retroviruses use CD169-mediated trans-infection of permissive lymphocytes to establish infection[J]. Science,2015,350(6260):563-567.
[12]	Walker JA, Smith KG. CD22: an inhibitory enigma[J]. Immunology, 2008,123(3):314-325.
[13]	Gjertsson I, Nitschke L, Tarkowski A. The role of B cell CD22 expression in Staphylococcus aureus arthritis and sepsis[J]. Microbes Infect,2004,6(4):377-382.
[14]	Jiang YN, Cai X, Zhou HM, et al. Diagnostic and prognostic roles of soluble CD22 in patients with Gram-negative bacterial sepsis[J]. Hepatobiliary Pancreat Dis Int,2015,14(5):523-529.
[15]	Jiang Y, Zhou H, Ma D, et al. MicroRNA-19a and CD22 comprise a feedback loop for B cell response in sepsis[J]. Med Sci Monit,2015,21:1548-1555.
[16]	Ma DY, Suthar MS, Kasahara S, et al. CD22 is required for protection against West Nile virus Infection[J]. J Virol,2013,87(6):3361-3375.
[17]	Nitschke L. Suppressing the antibody response with Siglec ligands[J]. N Engl J Med,2013,369(14):1373-1374.
[18]	Kreitman RJ, Squires DR, Stetler-Stevenson M, et al. PhaseⅠtrial of recombinant immunotoxin RFB4 (dsFv)-PE38 (BL22) in patients with B-cell malignancies[J]. J Clin Oncol,2005,23(27):6719-6729.
[19]	Shao JY, Yin WW, Zhang QF, et al. Siglec-7 defines a highly functional natural killer cell subset and inhibits cell-mediated activities[J]. Scand J Immunol,2016,84(3):182-190.
[20]	Mizrahi S, Gibbs BF, Karra L, et al. Siglec-7 is an inhibitory receptor on human mast cells and basophils[J]. J Allergy Clin Immunol,2014,134(1):230-233.
[21]	Nguyen KA, Hamzeh-Cognasse H, Palle S, et al. Role of Siglec-7 in apoptosis in human platelets[J]. PLoS One,2014,9(9):e106239.
[22]	Grutkoski PS, Chen Y, Chung CS, et al. Sepsis-induced SOCS-3 expression is immunologically restricted to phagocytes[J]. J Leukoc Biol,2003,74(5):916-922.
[23]	Orr SJ, Morgan NM, Buick RJ, et al. SOCS3 targets Siglec 7 for proteasomal degradation and blocks Siglec 7-mediated responses[J]. J Biol Chem,2007,282(6):3418-3422.
[24]	Varchetta S, Brunetta E, Roberto A, et al. Engagement of Siglec-7 receptor induces a pro-inflammatory response selectively in monocytes[J]. PLoS One,2012,7(9):e45821.
[25]	Siddiqui S, Schwarz F, Springer S, et al. Studies on the detection, expression, glycosylation, dimerization, and ligand binding properties of mouse Siglec-E[J]. J Biol Chem,2017,292(3):1029-1037.
[26]	Liu YC, Zou XB, Chai YF, et al. Macrophage polarization in inflammatory diseases[J]. Int J Biol Sci,2014,10(5):520-529.
[27]	Liu YC, Yao FH, Chai YF, et al. Xuebijing injection promotes M2 polarization of macrophages and improves survival rate in septic mice[J]. Evid Based Complement Alternat Med,2015,2015:352642.
[28]	Higuchi H, Shoji T, Murase Y, et al. Siglec-9 modulated IL-4 responses in the macrophage cell line RAW264[J]. Biosci Biotechnol Biochem,2016,80(3):501-509.
[29]	Higuchi H, Shoji T, Iijima S, et al. Constitutively expressed Siglec-9 inhibits LPS-induced CCR7, but enhances IL-4-induced CD200R expression in human macrophages[J]. Biosci Biotechnol Biochem,2016,80(6):1141-1148.
[30]	Chen GY, Brown NK, Wu W, et al. Broad and direct interaction between TLR and Siglec families of pattern recognition receptors and its regulation by Neu1[J]. Elife,2014,3:e04066.
[31]	Boyd CR, Orr SJ, Spence S, et al. Siglec-E is up-regulated and phosphorylated following lipopolysaccharide stimulation in order to limit TLR-driven cytokine production[J]. J Immunol, 2009,183(12):7703-7709.
[32]	Wu Y, Ren D, Chen GY. Siglec-E negatively regulates the activation of TLR4 by controlling its endocytosis[J]. J Immunol,2016,197(8): 3336-3347.
[33]	McMillan SJ, Sharma RS, Richards HE, et al. Siglec-E promotesβ2-integrin-dependent NADPH oxidase activation to suppress neutrophil recruitment to the lung[J]. J Biol Chem,2014,289(29):20370-20376.
[34]	Aalto K, Autio A, Kiss EA, et al. Siglec-9 is a novel leukocyte ligand for vascular adhesion protein-1 and can be used in PET imaging of inflammation and cancer[J]. Blood,2011,118(13):3725-3733.
[35]	Spence S, Greene MK, Fay F, et al. Targeting Siglecs with a sialic acid-decorated nanoparticle abrogates inflammation[J]. Sci Transl Med,2015,7(303):303ra140.
[36]	Chu S, Zhu X, You N, et al. The Fab fragment of a human anti-Siglec-9 monoclonal antibody suppresses LPS-induced inflammatory responses in human macrophages[J]. Front Immunol,2016,7:649-661.
[37]	Chen GY, Brown NK, Zheng P, et al. Siglec-G/10 in self-nonself discrimination of innate and adaptive immunity[J]. Glycobiology, 2014,24(9):800-806.
[38]	Stephenson HN, Mills DC, Jones H, et al. Pseudaminic acid onCampylobacter jejuniflagella modulates dendritic cell IL-10 expression via Siglec-10 receptor: a novel flagellin-host interaction[J]. J Infect Dis,2014,210(9):1487-1498.
[39]	Chen W, Han C, Xie B, et al. Induction of Siglec-G by RNA viruses inhibits the innate immune response by promoting RIG-I degradation[J]. Cell,2013,152(3):467-478.
[1]	Schauer R. Sialic acids as regulators of molecular and cellular interactions[J]. Curr Opin Struct Biol,2009,19(5):507-514.
[2]	Macauley MS, Crocker PR, Paulson JC.Siglec-mediated regulation of immune cell function in disease[J]. Nat Rev Immunol,2014,14(10):653-666.
[3]	Cao H, de Bono B, Belov K, et al. Comparative genomics indicates the mammalian CD33rSiglec locus evolved by an ancient large-scale inverse duplication and suggests all Siglecs share a common ancestral region[J]. Immunogenetics,2009,61(5):401-417.
[40]	Parlato M, Souza-Fonseca-Guimaraes F, Philippart F, et al. CD24-triggered caspase-dependent apoptosis via mitochondrial membrane depolarization and reactive oxygen species production of human neutrophils is impaired in sepsis[J]. J Immunol,2014,192(5):2449-2459.
[41]	Chen GY, Tang J, Zheng P, et al. CD24 and Siglec-10 selectively repress tissue damage-induced immune responses[J].Science, 2009,323(5922):1722-1725.
[42]	Chen GY, Chen X, King S, et al. Amelioration of sepsis by inhibiting sialidase-mediated disruption of the CD24-Siglec-G interaction[J]. Nat Biotechnol,2011,29(5):428-435.
[43]	Paulson JC, Kawasaki N. Sialidase inhibitors DAMPen sepsis[J]. Nat Biotechnol,2011,29(5):406-407.
[44]	Ding Y, Guo Z, Liu Y, et al. The lectin Siglec-G inhibits dendritic cell cross-presentation by impairing MHC classⅠ-peptide complex formation[J]. Nat Immunol,2016,17(10):1167-1175.
[45]	Bandala-Sanchez E, Zhang Y, Reinwald S, et al. T cell regulation mediated by interaction of soluble CD52 with the inhibitory receptor Siglec-10[J]. Nat Immunol,2013,14(7):741-748.
[46]	Nitschke L. Siglec-G is a B-1 cell inhibitory receptor and also controls B cell tolerance[J]. Ann N Y Acad Sci,2015,1362:117-121.
[47]	Jellusova J, Düber S, Gückel E, et al. Siglec-G regulates B1 cell survival and selection[J]. J Immunol,2010,185(6):3277-3284.
[48]	Carlin AF, Chang YC, Areschoug T, et al. Group BStreptococcus suppression of phagocyte functions by protein-mediated engagement of human Siglec-5[J]. J Exp Med,2009,206(8):1691-1699.
[49]	Ali SR, Fong JJ, Carlin AF, et al. Siglec-5 and Siglec-14 are polymorphic paired receptors that modulate neutrophil and amnion signaling responses to group BStreptococcus[J]. J Exp Med,2014,211(6):1231-1242.
[50]	Angata T, Ishii T, Motegi T, et al. Loss of Siglec-14 reduces the risk of chronic obstructive pulmonary disease exacerbation[J]. Cell Mol Life Sci,2013,70(17):3199-3210.
[51]	Wielgat P, Mroz RM, Stasiak-Barmuta A, et al. Inhaled corticosteroids increase siglec-5/14 expression in sputum cells of COPD patients[J].Adv Exp Med Biol,2015,839:1-5.
[4]	Rhodes A, Evans LE, Alhazzani W, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock: 2016[J]. Crit Care Med,2017,45(3):486-552.
[5]	Boomer JS, To K, Chang KC, et al. Immunosuppression in patients who die of sepsis and multiple organ failure[J]. JAMA,2011,306(23):2594-2605.
[6]	Izquierdo-Useros N, Lorizate M, Contreras FX, et al. Sialyllactose in viral membrane gangliosides is a novel molecular recognition pattern for mature dendritic cell capture of HIV-1[J]. PLoS Biol,2012,10(4):e1001315.
[7]	Gummuluru S, Pina RNG, Akiyama H. CD169-dependent cell-associated HIV-1 transmission: a driver of virus dissemination[J]. J Infect Dis,2014,210 (Suppl 3):S641-S647.
[8]	Gupta P, Lai SM, Sheng J, et al. Tissue-resident CD169(+) macrophages form a crucial front line against plasmodium Infection[J]. Cell Rep,2016,16(6):1749-1761.
[9]	Shaabani N, Duhan V, Khairnar V, et al. CD169⁺macrophages regulate PD-L1 expression via type I interferon and thereby prevent severe immunopathology after LCMV infection[J]. Cell Death Dis,2016,7(11):e2446.

Please choose a citation manager

Content to export