Role of monocytes in immunopathogenesis of infectious and inflammatory diseases: from theory to practice

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Abstract

Monocytes are circulating blood cells derived from bone marrow. They are the body’s first line of defense against pathogens and are involved in immune responses against viruses, bacteria, fungi and parasites invasion. For a long time, monocytes were considered a homogeneous group of cells, but then by means of flow cytometry development it was shown that they can be divided into three subpopulations according to surface molecules CD14 and CD16 expression: classical (CD14++CD16–), proinflammatory (CD14+CD16++) and intermediate (CD14++CD16+). This review focuses on various mechanisms of an implementation of the functional activity of various monocytes subpopulations and their impairment in various viral diseases, bacterial infections and sepsis.

About the authors

Andrey S. Trulioff

Institute of Experimental Medicine

Author for correspondence.
Email: trulioff@gmail.com
ORCID iD: 0000-0002-7495-446X
SPIN-code: 8688-7506

Cand. Sci. (Biology), Senior Research Associate of Department of Immunology

Russian Federation, 12 Academician Pavlov St., Saint Petersburg, 197022

Alexandr G. Borisov

Krasnoyarsk Science Center of the SB RAS

Email: 2410454@mail.ru
ORCID iD: 0000-0001-6930-3243
SPIN-code: 9570-2254

Institute of Medical Problems of the North, MD, Cand. Sci. (Medicine), Leading Research Associate of Laboratory of Cell and Mollecular Phisiology and Patology

Russian Federation, Krasnoyarsk

Igor V. Kudriavtsev

Institute of Experimental Medicine

Email: igorek1981@yandex.ru
ORCID iD: 0000-0001-7204-7850
SPIN-code: 4903-7636

Cand. Sci. (Biology), Head of Laboratory of Cell Immunology

Russian Federation, 12 Academician Pavlov St., Saint Petersburg, 197022

Vladimir A. Lazanovich

EUROMED Clinik

Email: immuno2003@mail.ru
ORCID iD: 0000-0003-0354-4890
SPIN-code: 1037-4447

MD, Cand. Sci. (Medicine), allergist-immunologist

Russian Federation, Krasnodar

Andrei A. Savchenko

Krasnoyarsk Science Center of the SB RAS

Email: aasavchenko@yandex.ru
ORCID iD: 0000-0001-5829-672X
SPIN-code: 3132-8260

Institute of Medical Problems of the North, MD, Dr. Sci (Medicine), Head of Cell and Mollecular Phisiology and Patology

Russian Federation, Krasnoyarsk

References

  1. Kasparov EhV, Savchenko AA, Kudlai DA, et al. Clinical immunology. Rehabilitation of the immune system . Krasnoyarsk: Versona; 2022. 196 p.
  2. Gren ST, Grip O. Role of monocytes and intestinal macrophages in Crohn’s disease and ulcerative colitis. Inflamm Bowel Dis. 2016;22(8)1992–1998. doi: 10.1097/MIB.0000000000000824
  3. Wallis ZK, Williams KC. Monocytes in HIV and SIV infection and aging: implications for inflamm-aging and accelerated aging. Viruses. 2022;14(2):409. doi: 10.3390/v14020409
  4. Cumakova SP, Urazova OI, Denisenko OA, et al. Cytokines in the mechanisms of regulation of monocytopoiesis in ischemic heart disease. Russian journal of hematology and transfusiology. 2022;67(4):511–524. EDN: FDACYA doi: 10.35754/0234-5730-2022-67-4-511-524
  5. Ożańska A, Szymczak D, Rybka J. Pattern of human monocyte subpopulations in health and disease. Scand J Immunol. 2020;92(1):e12883. doi: 10.1111/sji.12883
  6. Liu S, Szatmary P, Lin JW, et al. Circulating monocytes in acute pancreatitis. Front Immunol. 2022;13:1062849. doi: 10.3389/fimmu.2022.1062849
  7. Orozco SL, Canny SP, Hamerman JA. Signals governing monocyte differentiation during inflammation. Curr Opin Immunol . 2021;73:16–24. doi: 10.1016/j.coi.2021.07.007
  8. Bettke JA, Tam JW, Montoya V, et al. Inflammatory monocytes promote granuloma-mediated control of persistent salmonella infection. Infect Immun. 2022;90(4):e0007022. doi: 10.1128/iai.00070-22
  9. Xiong H, Pamer EG. Monocytes and infection: modulator, messenger and effector. Immunobiology. 2015;220(2):210–214. doi: 10.1016/j.imbio.2014.08.007
  10. Samstein M, Schreiber HA, Leiner IM, et al. Essential yet limited role for CCR2 + inflammatory monocytes during Mycobacterium tuberculosis -specific T cell priming. Elife . 2013;2:e01086. doi: 10.7554/eLife.01086
  11. Zhang Y, Khairallah C, Sheridan BS, et al. CCR2 + inflammatory monocytes are recruited to Yersinia pseudotuberculosis pyogranulomas and dictate adaptive responses at the expense of innate immunity during oral infection. Infect Immun. 2018;86(3):e00782–17. doi: 10.1128/IAI.00782-17
  12. Auger JP, Rivest S, Benoit-Biancamano MO, et al. Inflammatory monocytes and neutrophils regulate Streptococcus suis -induced systemic inflammation and disease but are not critical for the development of central nervous system disease in a mouse model of infection. Infect Immun. 2020;88(3):e00787–19. doi: 10.1128/IAI.00787-19
  13. Montaño DE, Hartung S, Wich M, et al. The TLR-NF-kB axis contributes to the monocytic inflammatory response against a virulent strain of Lichtheimia corymbifera , a causative agent of invasive mucormycosis. Front Immunol. 2022;13:882921. doi: 10.3389/fimmu.2022.882921
  14. Sabbatinelli J, Matacchione G, Giuliani A, et al. Circulating biomarkers of inflammaging as potential predictors of COVID-19 severe outcomes. Mech Ageing Dev. 2022;204:111667. doi: 10.1016/j.mad.2022.111667
  15. Passlick B, Flieger D, Ziegler-Heitbrock HW. Identification and characterization of a novel monocyte subpopulation in human peripheral blood. Blood. 1989;74(7):2527–2534. doi: 10.1182/blood.V74.7.2527.2527
  16. Ziegler-Heitbrock HW, Passlick B, Flieger D. The monoclonal antimonocyte antibody My4 stains B lymphocytes and two distinct monocyte subsets in human peripheral blood. Hybridoma. 1988;7(6):521–527. doi: 10.1089/hyb.1988.7.521
  17. Wright SD, Ramos RA, Tobias PS, et al. CD14, a receptor for complexes of lipopolysaccharide (LPS) and LPS binding protein. Science. 1990;249(4975):1431–1433. doi: 10.1126/science.1698311
  18. Li L, Cai W, Guo P, et al. Characteristics and clinical significance of plasma IL-18, sCD14, and sCD163 levels in patients with HIV-1 infection. J Med Virol. 2023;95(1):e28223. doi: 10.1002/jmv.28223
  19. Maddaloni C, De Rose DU, Santisi A, et al. The emerging role of presepsin (P-SEP) in the diagnosis of sepsis in the critically ill infant: a literature review. Int J Mol Sci. 2021;22(22):12154. doi: 10.3390/ijms222212154
  20. Hsieh WT, Hsu MH, Lin WJ, et al. Ergosta-7, 9 (11), 22-trien-3β-ol Interferes with LPS docking to LBP, CD14, and TLR4/MD-2 Co-receptors to attenuate the NF-κB inflammatory pathway in vitro and drosophila. Int J Mol Sci. 2021;22(12):6511. doi: 10.3390/ijms22126511
  21. Gonzalez JC, Chakraborty S, Thulin NK, Wang TT. Heterogeneity in IgG-CD16 signaling in infectious disease outcomes. Immunol Rev. 2022;309(1):64–74. doi: 10.1111/imr.13109
  22. Fall AKDJ, Dechavanne C, Sabbagh A, et al. Combined polymorphisms involving the IgG heavy chain and Fc gamma receptors among Fulani and non-Fulani in Benin: implications for the natural protection of young Fulani against Plasmodium falciparum malaria infections. Infect Genet Evol. 2023;112:105461. doi: 10.1016/j.meegid.2023.105461
  23. Nasr A, Aljada A, Hamid O, et al. Significant differences in FcγRIIa , FcγRIIIa and FcγRIIIb genes polymorphism and anti-malarial IgG subclass pattern are associated with severe Plasmodium falciparum malaria in Saudi children. Malar J. 2021;20(1):376. doi: 10.1186/s12936-021-03901-0
  24. Shimizu Y, Kohyama M, Yorifuji H, et al. FcγRIIIA-mediated activation of NK cells by IgG heavy chain complexed with MHC class II molecules. Int Immunol. 2019;31(5):303–314. doi: 10.1093/intimm/dxz010
  25. Treffers LW, van Houdt M, Bruggeman CW, et al. FcγRIIIb restricts antibody-dependent destruction of cancer cells by human neutrophils. Front Immunol. 2019;(9):3124. doi: 10.3389/fimmu.2018.03124
  26. Hellman L. Phenotypic and functional heterogeneity of monocytes and macrophages. Int J Mol Sci. 2023;24(19):14525. doi: 10.3390/ijms241914525
  27. Williams H, Mack C, Baraz R, et al. Monocyte differentiation and heterogeneity: inter-subset and interindividual differences. Int J Mol Sci. 2023;24(10):8757. doi: 10.3390/ijms24108757
  28. Buscher K, Marcovecchio P, Hedrick CC, Ley K. Patrolling mechanics of non-classical monocytes in vascular inflammation. Front Cardiovasc Med. 2017;4:80. doi: 10.3389/fcvm.2017.00080
  29. Gabriel H, Urhausen A, Brechtel L, et al. Alterations of regular and mature monocytes are distinct, and dependent of intensity and duration of exercise. Eur J Appl Physiol Occup Physiol. 1994;69(2):179–181. doi: 10.1007/BF00609414
  30. Slavick A, Furer V, Polachek A, et al. Circulating and synovial monocytes in arthritis and ex-vivo model to evaluate therapeutic modulation of synovial monocytes. Immunol Invest. 2023;52(7):832–855. doi: 10.1080/08820139.2023.2247438
  31. Tamene W, Marconi VC, Abebe M, et al. Differential expression of chemokine receptors on monocytes in TB and HIV S. Heliyon. 2023;9(6):e17202. doi: 10.1016/j.heliyon.2023.e17202
  32. Bianconi V, Sahebkar A, Atkin SL, Pirro M. The regulation and importance of monocyte chemoattractant protein-1. Curr Opin Hematol. 2018:25(1):44–51. doi: 10.1097/MOH.0000000000000389
  33. Patysheva MR, Stakheeva MN, Larionova IV, et al. Monocytes and cancer: promising role as a diagnostic marker and application in therapy. Bulletin of Siberian Medicine. 2019;18(1):60–75. EDN: ARRYLN doi: 10.20538/1682-0363-2019-1-60-75
  34. Jarosova R, Ondrackova P, Leva L, et al. Cytokine expression by CD163 + monocytes in healthy and Actinobacillus pleuropneumoniae -infected pigs. Res Vet Sci. 2022;152:1–9. doi: 10.1016/j.rvsc.2022.07.015
  35. Lee JG, Jaeger KE, Seki Y, et al. Human CD36hi monocytes induce Foxp3 + CD25 + T cells with regulatory functions from CD4 and CD8 subsets. Immunology. 2021:163(3):293–309. doi: 10.1111/imm.13316
  36. Qu PF, Li R, Xu C, et al. A clinical pilot study to evaluate CD64 expression on blood monocytes as an indicator of periprosthetic joint infection. J Bone Joint Surg Am. 2020;102(17):e99. doi: 10.2106/JBJS.20.00057
  37. Lekka K, Marangos M, Roupas N, et al. Evaluation of the activity of neutrophils and monocytes in diabetic patients with sepsis, can surface antigens HLA-DR and CD64 be useful as prognostic factors? J Clin Med Res. 2020;12(3):157–164. doi: 10.14740/jocmr4068
  38. Savchenko AA, Borisov AG, Modestov AA, et al. Monocytes subpopulations and chemiluminescent activity in patients with renal cell carcinoma. Medical immunoljgy . 2015;17(2):141–150. EDN: TORDFB doi: 10.15789/1563-0625-2015-2-141-150
  39. Novais FO, Nguyen BT, Beiting DP, et al. Human classical monocytes control the intracellular stage of Leishmania braziliensis by reactive oxygen species. J Infect Dis. 2014;209(8):1288–1296. doi: 10.1093/infdis/jiu013
  40. Zawada AM, Rogacev KS, Rotter B, et al. SuperSAGE evidence for CD14 ++ CD16 + monocytes as a third monocyte subset. Blood. 2011;118(12):e50–e61. doi: 10.1182/blood-2011-01-326827
  41. Cros J, Cagnard N, Woollard K, et al. Human CD14dim monocytes patrol and sense nucleic acids and viruses via TLR7 and TLR8 receptors. Immunity. 2010;33(3):375–386. doi: 10.1016/j.immuni.2010.08.012
  42. Urbán-Solano A, Flores-Gonzalez J, Cruz-Lagunas A, et al. High levels of PF4, VEGF-A, and classical monocytes correlate with the platelets count and inflammation during active tuberculosis. Front Immunol. 2022;13:1016472. doi: 10.3389/fimmu.2022.1016472
  43. Lira-Junior R, Holmström SB, Clark R, et al. S100A12 expression is modulated during monocyte differentiation and reflects periodontitis severity. Front Immunol. 2020;11:86. doi: 10.3389/fimmu.2020.00086
  44. Gaur P, Myles A, Misra R, Aggarwal A. Intermediate monocytes are increased in enthesitis-related arthritis, a category of juvenile idiopathic arthritis. Clin Exp Immunol. 2017;187(2):234–241. doi: 10.1111/cei.12880
  45. Connaughton EP, Naicker S, Hanley SA, et al. Phenotypic and functional heterogeneity of human intermediate monocytes based on HLA-DR expression. Immunol Cell Biol. 2018;5:45. doi: 10.1111/imcb.12032
  46. Narasimhan PB, Marcovecchio P, Hamers AAJ, Hedrick CC. Nonclassical monocytes in health and disease. Annu Rev Immunol . 2019;37:439–456. doi: 10.1146/annurev-immunol-042617-053119
  47. Marcovecchio PM, Zhu YP, Hanna RN, et al. Frontline science: Kindlin-3 is essential for patrolling and phagocytosis functions of nonclassical monocytes during metastatic cancer surveillance. J Leukoc Biol. 2020;107(6):883–892. doi: 10.1002/JLB.4HI0420-098R
  48. Radzyukevich YV, Kosyakova NI, Prokhorenko IR. Participation of monocyte subpopulations in progression of experimental endotoxemia (EE) and systemic inflammation. J Immunol Res. 2021;2021:1762584. doi: 10.1155/2021/1762584
  49. Cormican S, Griffin MD. Human monocyte subset distinctions and function: insights from gene expression analysis. Front Immunol. 2020;11:1070. doi: 10.3389/fimmu.2020.01070
  50. Kapellos TS, Bonaguro L, Gemünd I, et sl. Human monocyte subsets and phenotypes in major chronic inflammatory diseases. Front Immunol. 2019;10:2035. doi: 10.3389/fimmu.2019.02035
  51. Lehman N, Kowalska W, Zarobkiewicz M, et al. Pro- vs. Anti-inflammatory features of monocyte subsets in glioma patients. Int J Mol Sci. 2023;24(3):1879. doi: 10.3390/ijms24031879
  52. Kalashnikova AA, Voroshilova TM, Chinenova LV, et al. Monocyte subsets in healthy adults and sepsis patients. Medical immunology. 2018;20(6):815–824. EDN: YOOZML doi: 10.15789/1563-0625-2018-6-815-824
  53. Sampath P, Moideen K, Ranganathan UD, Bethunaickan R. Monocyte subsets: phenotypes and function in tuberculosis infection. Front Immunol. 2018;9:1726. doi: 10.3389/fimmu.2018.01726
  54. Rambaran S, Maseko TG, Lewis L, et al. Blood monocyte and dendritic cell profiles among people living with HIV with Mycobacterium tuberculosis co-infection. BMC Immunol. 2023;24(1):21. doi: 10.1186/s12865-023-00558-z
  55. Zhang ML, Jiang YF, Wang XR, et al. Different phenotypes of monocytes in patients with new-onset mild acute pancreatitis. World J Gastroenterol. 2017;23(8):1477–1488. doi: 10.3748/wjg.v23.i8.1477
  56. Zheng J, Fan J, Huang C, et al. Dynamic detection of monocyte subsets in peripheral blood of patients with acute hypertriglyceridemic pancreatitis. Gastroenterol Res Pract. 2019;2019:5705782. doi: 10.1155/2019/5705782
  57. Zhang M, Ding L, Wang X, et al. Circulating CD14 + CD163 + CD115 + M2 monocytes are associated with the severity of new onset severe acute pancreatitis in Chinese patients. Int Immunopharmacol. 2018;57:181–189. doi: 10.1016/j.intimp.2018.02.018
  58. Grainger JR, Wohlfert EA, Fuss IJ, et al. Inflammatory monocytes regulate pathologic responses to commensals during acute gastrointestinal infection. Nat Med. 2013;19(6):713–721. doi: 10.1038/nm.3189
  59. Yang J, Qiao M, Li Y, et al. Expansion of a population of large monocytes (atypical monocytes) in peripheral blood of patients with acute exacerbations of chronic obstructive pulmonary diseases. Mediators Inflamm. 2018;2018:9031452. doi: 10.1155/2018/9031452
  60. Gudenschwager Basso EK, Ju J, Soliman E, et al. Immunoregulatory and neutrophil-like monocyte subsets with distinct single-cell transcriptomic signatures emerge following brain injury. J Neuroinflammation . 2024;21(1):41. doi: 10.1186/s12974-024-03032-8
  61. Ikeda N, Kubota H, Suzuki R, et al. The early neutrophil-committed progenitors aberrantly differentiate into immunoregulatory monocytes during emergency myelopoiesis. Cell Rep. 2023;42(3):112165. doi: 10.1016/j.celrep.2023.112165 .
  62. Wiencke JK, Nissen E, Koestler DC, et al. Enrichment of a neutrophil-like monocyte transcriptional state in glioblastoma myeloid suppressor cells. // Res Sq [Preprint]. 2023:rs.3.rs–3793353. doi: 10.21203/rs.3.rs-3793353/v1
  63. Brown B, Ojha V, Fricke I, et al. Innate and adaptive immunity during SARS-CoV-2 infection: biomolecular cellular markers and mechanisms. Vaccines (Basel). 2023;11(2):408. doi: 10.3390/vaccines11020408
  64. Kudryavtsev I, Rubinstein A, Golovkin A, et al. Dysregulated immune responses in SARS-CoV-2-infected patients: a comprehensive overview. Viruses. 2022;(5):1082. doi: 10.3390/v14051082
  65. Zhang D, Guo R, Lei L, et al. Frontline Science: COVID-19 infection induces readily detectable morphologic and inflammation-related phenotypic changes in peripheral blood monocytes. J Leukoc Biol. 2021;109(1):13–22. doi: 10.1002/JLB.4HI0720-470R
  66. Zhou Z, Ren L, Zhang L, et al. Heightened innate immune responses in the respiratory tract of COVID-19 patients. Cell Host Microbe. 2020;27(6):883–890.e2. doi: 10.1016/j.chom.2020.04.017
  67. Mann ER, Menon M, Knight SB, et al. Longitudinal immune profiling reveals key myeloid signatures associated with COVID-19. Sci Immunol. 2020;5(51):eabd6197. doi: 10.1126/sciimmunol.abd6197
  68. Giamarellos-Bourboulis EJ, Netea MG, Rovina N, et al. Complex immune dysregulation in COVID-19 patients with severe respiratory failure. Cell Host Microbe . 2020;27(6):992–1000.e3 . doi: 10.1016/j.chom.2020.04.009
  69. Kuri-Cervantes L, Pampena MB, Meng W, et al. Comprehensive mapping of immune perturbations associated with severe COVID-19. Sci Immunol. 2020;5(49):eabd7114. doi: 10.1126/sciimmunol.abd7114
  70. Arunachalam PS, Wimmers F, Mok CKP, et al. Systems biological assessment of immunity to mild versus severe COVID -19 infection in humans. Science. 2020;369(6508):1210–1220. doi: 10.1126/science.abc6261
  71. Guo C, Li B, Ma H, et al. Single-cell analysis of two severe COVID-19 patients reveals a monocyte-associated and tocilizumab-responding cytokine storm. Nat Commun. 2020;11(1):3924. doi: 10.1038/s41467-020-17834-w
  72. Guilliams M, Mildner A, Yona S. Developmental and functional heterogeneity of monocytes. Immunity. 2018;49(4):595–613. doi: 10.1016/j.immuni.2018.10.005
  73. Laing AG, Lorenc A, Del Molino Del Barrio I., et al. A dynamic COVID -19 immune signature includes associations with poor prognosis. Nat Med. 2020;26(10):1623–1635. doi: 10.1038/s41591-020-1038-6
  74. Wilk AJ, Rustagi A, Zhao NQ, et al. A single-cell atlas of the peripheral immune response in patients with severe COVID-19. Nat Med. 2020;26(7):1070–1076. doi: 10.1038/s41591-020-0944-y
  75. Silvin A, Chapuis N, Dunsmore G, et al. Elevated calprotectin and abnormal myeloid cell subsets discriminate severe from mild COVID-19. Cell . 2020;182(6):1401–1418.e18. doi: 10.1016/j.cell.2020.08.002
  76. Chilunda V, Martinez-Aguado P, Xia LC, et al. Transcriptional changes in CD16 + monocytes may contribute to the pathogenesis of COVID-19. Front Immunol. 2021;12:665773. doi: 10.3389/fimmu.2021.665773
  77. Schulte-Schrepping J, Reusch N, Paclik D, et al. Suppressive myeloid cells are a hallmark of severe COVID-19. MedRxiv . 2020. doi: 10.1101/2020.06.03.20119818
  78. Gómez-Rial J, Currás-Tuala MJ, Rivero-Calle I, et al. Increased serum levels of sCD14 and sCD163 indicate a preponderant role for monocytes in COVID-19 immunopathology. Front Immunol . 2020;11:560381. doi: 10.3389/fimmu.2020.560381
  79. Monneret G, Lepape A, Voirin N, et al. Persisting low monocyte human leukocyte antigen-DR expression predicts mortality in septic shock. Intensive Care Med. 2006;32:1175–1183. doi: 10.1007/s00134-006-0204-8
  80. Bronte V, Brandau S, Chen SH, et al. Recommendations for myeloid-derived suppressor cell nomenclature and characterization standards. Nat Commun. 2016;7(1):12150. doi: 10.1038/ncomms12150
  81. Xu G, Qi F, Li H, et al. The differential immune responses to COVID -19 in peripheral and lung revealed by single-cell RNA sequencing. Cell Discov . 2020;6(1):73. doi: 10.1038/s41421-020-00225-2
  82. Hopkins FR, Govender M, Svanberg C, et al. Major alterations to monocyte and dendritic cell subsets lasting more than 6 months after hospitalization for COVID-19. Front Immunol . 2023;13:1082912. doi: 10.3389/fimmu.2022.1082912
  83. Ohno Y, Kitamura H, Takahashi N, et al. IL-6 down-regulates HLA class II expression and IL-12 production of human dendritic cells to impair activation of antigen-specific CD4 + T cells. Cancer Immunol Immunother. 2016;65:193–204. doi: 10.1007/s00262-015-1791-4
  84. Ivashkin VT, Chulanov VP, Mamonova NA, et al. Clinical Practice Guidelines of the Russian Society for the Study of the Liver, the Russian Gastroenterological Association, the National Scientific Society of Infectious Disease Specialists for the Diagnosis and Treatment of Chronic Hepatitis C. Russian Journal of Gastroenterology, Hepatology, Coloproctology . 2023;33(1):84–124. EDN: IUKGIX doi: 10.22416/1382-4376-2023-33-1-84-124
  85. Tsukanov VV, Savchenko AA, Cherepnin MA, et al. Association of blood NK cell phenotype with the severity of liver fibrosis in patients with chronic viral hepatitis c with genotype 1 or 3. Diagnostics . 2024;14(5):472. doi: 10.3390/diagnostics14050472
  86. Lee MH, Chen YT, Huang YH, et al. Chronic viral hepatitis B and c outweigh MASLD in the associated risk of cirrhosis and HCC. Clin Gastroenterol Hepatol. 2024;22(6):1275–1285e2. doi: 10.1016/j.cgh.2024.01.045
  87. Schlaak JF. Current therapy of chronic viral hepatitis B, C and D. J Pers Med. 2023;13(6):964. doi: 10.3390/jpm13060964
  88. Chen C, Cai H, Shen J, et al. Exploration of a hypoxia-immune-related microenvironment gene signature and prediction model for hepatitis C-induced early-stage fibrosis. J Transl Med. 2024;22(1):116. doi: 10.1186/s12967-024-04912-6
  89. Ferrasi AC, Lima SVG, Galvani AF, et al. Metabolomics in chronic hepatitis C: Decoding fibrosis grading and underlying pathways. World J Hepatol. 2023;15(11):1237–1249. doi: 10.4254/wjh.v15.i11.1237
  90. Sellau J, Puengel T, Hoenow S, et al. Monocyte dysregulation: consequences for hepatic infections. Semin Immunopathol. 2021;(N):493–506. doi: 10.1007/s00281-021-00852-1
  91. Song H, Tan G, Yang Y, et al. Hepatitis B virus-induced imbalance of inflammatory and antiviral signaling by differential phosphorylation of STAT1 in human monocytes. J Immunol. 2019;202(8):2266–2275. doi: 10.4049/jimmunol.1800848
  92. Geng A, Flint E, Bernsmeier C. Plasticity of monocytes and macrophages in cirrhosis of the liver. Front Netw Physiol. 2022;2:937739. doi: 10.3389/fnetp.2022.937739
  93. Tan-Garcia A, Lai F, Sheng Yeong JP, et al. Liver fibrosis and CD206 + macrophage accumulation are suppressed by anti-GM-CSF therapy. JHEP Rep. 2019;2(1)100062. doi: 10.1016/j.jhepr.2019.11.006
  94. Riad NM, AbdEl Ghaffar HA, Mansour RR, et al. Clinical significance of evaluation of monocytic receptors in patients with hepatitis c virus infection. Viral Immunol. 2023;36(7):475–483. doi: 10.1089/vim.2022.0180
  95. Ali F, Hammad R, Kotb FM, et al. Flow cytometry assessment of monocyte subsets alteration in hepatocellular carcinoma post hepatitis C virus infection. Egypt J Immunol. 2022;29(4):33–45.
  96. Leplina OY, Tikhonova MA, Meledina IV, et al. Topical issues of clinical symptoms and diagnostics of septic shock. Russian Journal of Infection and Immunity . 2022;12(3):475–485. EDN: EPFQUA doi: 10.15789/2220-7619-CMS-1810
  97. Hernández-Sarmiento LJ, Valdés-López JF, Urcuqui-Inchima S. American-Asian- and African lineages of Zika virus induce differential pro-inflammatory and Interleukin 27-dependent antiviral responses in human monocytes. Virus Res. 2023;325:199040. doi: 10.1016/j.virusres.2023.199040
  98. Michlmayr D, Andrade P, Gonzalez K, et al. CD14 + CD16 + monocytes are the main target of Zika virus infection in peripheral blood mononuclear cells in a paediatric study in Nicaragua. Nat Microbiol. 2017;2(11):1462–1470. doi: 10.1038/s41564-017-0035-0
  99. Serman TM, Gack MU. Evasion of innate and intrinsic antiviral pathways by the Zika virus. Viruses . 2019;11(10):970. doi: 10.3390/v11100970
  100. Savchenko AA, Martynova GP, Ikkes LA, et al. Changes in in vitro GM-CSF-exposured monocyte subset composition and phagocytic activity in children with infectious mononucleosis. Russian Journal of Infection and Immunity. 2023;13(3):446–456 . EDN: OITDKO doi: 10.15789/2220-7619-CII-4666
  101. Jog NR, Chakravarty EF, Guthridge JM, James JA. Epstein barr virus interleukin 10 suppresses anti-inflammatory phenotype in human monocytes. Front Immunol . 2018;9:2198. doi: 10.3389/fimmu.2018.02198
  102. Xu X, Zhu N, Zheng J, et al. EBV abortive lytic cycle promotes nasopharyngeal carcinoma progression through recruiting monocytes and regulating their directed differentiation. PLoS Pathog. 2024;20(1):e1011934. doi: 10.1371/journal.ppat.1011934
  103. Chen M, Yu S, Gao Y, et al. TRAF6-TAK1-IKKβ pathway mediates TLR2 agonists activating “one-step” NLRP3 inflammasome in human monocytes. Cytokine . 2023;169:156302. doi: 10.1016/j.cyto.2023.156302
  104. Dimitrov E, Halacheva K, Minkov G, et al. Prediction of outcome using CD14 ++ CD16 – , CD14 ++ CD16 + and CD14 + CD16 ++ monocyte subpopulations in patients with complicated intra-abdominal infections. Med Microbiol Immunol. 2023;212(5):381–390. doi: 10.1007/s00430-023-00779-4
  105. Lauvau G, Loke P, Hohl TM. Monocyte-mediated defense against bacteria, fungi, and parasites. Semin Immunol. 2015;27(6):397–409 . doi: 10.1016/j.smim.2016.03.014
  106. Cloots RH, Sankaranarayanan S, de Theije CC, et al. Ablation of Arg1 in hematopoietic cells improves respiratory function of lung parenchyma, but not that of larger airways or inflammation in asthmatic mice. Am J Physiol Lung Cell Mol Physiol. 2013;305(5):L364–3L76. doi: 10.1152/ajplung.00341.2012
  107. Hoenow S, Yan K, Noll J, et al. The properties of proinflammatory Ly6Chi monocytes are differentially shaped by parasitic and bacterial liver infections. Cells . 2022;11(16):2539. doi: 10.3390/cells11162539
  108. Andrade-Oliveira V, Foresto-Neto O, Watanabe IKM, et al. Inflammation in renal diseases: new and old players. Front Pharmacol. 2019;10:1192. doi: 10.3389/fphar.2019.01192
  109. Biram A, Liu J, Hezroni H, et al. Bacterial infection disrupts established germinal center reactions through monocyte recruitment and impaired metabolic adaptation. Immunity. 2022;55(3):442–458.e8. doi: 10.1016/j.immuni.2022.01.013
  110. Park MY, Kim HS, Jeong YS, et al. Novel Sca-1 + macrophages modulate the pathogenic progress of endotoxemia. Biochem Biophys Res Commun. 2020;533(1):83–89. doi: 10.1016/j.bbrc.2020.08.118
  111. Popescu M, Cabrera-Martinez B, Winslow GM. TNF-α contributes to lymphoid tissue disorganization and germinal center B Cell suppression during intracellular bacterial infection. J Immunol. 2019;203(9):2415–2424. doi: 10.4049/jimmunol.1900484
  112. Wang G, Zhao H, Zheng B, et al. TLR2 promotes monocyte/macrophage recruitment into the liver and microabscess formation to limit the spread of Listeria monocytogenes . Front Immunol. 2019;10:1388. doi: 10.3389/fimmu.2019.01388 .
  113. McLaughlin PA, Bettke JA, Tam JW, et al. Inflammatory monocytes provide a niche for Salmonella expansion in the lumen of the inflamed intestine. PLoS Pathog. 2019;15(7):e1007847. doi: 10.1371/journal.ppat.1007847
  114. Shima Y, Masuda T, Miwa N, et al. Monocytes predict prognosis and successful treatment in older patients with miliary tuberculosis. J Clin Tuberc Other Mycobact Dis. 2024;35:100437. doi: 10.1016/j.jctube.2024.100437
  115. Luo M, Zou X, Zeng Q, et al. Monocyte at diagnosis as a prognosis biomarker in tuberculosis patients with anemia. Front Med (Lausanne). 2023;10:1141949. doi: 10.3389/fmed.2023.1141949
  116. Wang W, Wang LF, Liu YY, et al. Value of the ratio of monocytes to lymphocytes for monitoring tuberculosis therapy. Can J Infect Dis Med Microbiol. 2019;2019:3270393. doi: 10.1155/2019/3270393
  117. Rao Muvva J, Parasa VR, Lerm M, et al. Polarization of human monocyte-derived cells with vitamin D promotes control of Mycobacterium tuberculosis infection. Front Immunol . 2020;10:3157. doi: 10.3389/fimmu.2019.03157
  118. Venet F, Demaret J, Gossez M, Monneret G. Myeloid cells in sepsis-acquired immunodeficiency. Ann N Y Acad Sci. 2021;1499(1):3–17. doi: 10.1111/nyas.14333
  119. Passos S, Carvalho LP, Costa RS, Campos TM. Intermediate monocytes contribute to pathologic immune response in Leishmania braziliensis infections. J Infect Dis. 2015;211(2):274–282. doi: 10.1093/infdis/jiu439
  120. Fingerle G, Pforte A, Passlick B, Blumenstein M. The novel subset of CD14 + /CD16 + blood monocytes is expanded in sepsis patients. Blood . 1993;82(10):3170–3176. doi: 10.1182/blood.V82.10.3170.3170
  121. Herra CM, Keane CT, Whelan A. Increased expression ofFcγ receptors on neutrophils and monocytes may reflect ongoing bacte-rial infection. J Med Microbiol. 1996;44:135–140. doi: 10.1099/00222615-44-2-135
  122. Nockher WA, Scherberich JE. Expanded CD14 + CD16 + monocyte subpopulation in patients with acute and chronic infectionsundergoing hemodialysis. Infect Immun. 1998;66:2782–2790. doi: 10.1128/iai.66.6.2782-2790.1998
  123. Liepelt A, Hohlstein P, Gussen H, Differential gene expression in circulating CD14( + ) monocytes indicates the prognosis of critically Ill patients with sepsis. J Clin Med. 2020;9(1):127. doi: 10.3390/jcm9010127
  124. Mukherjee R, Kanti Barman P, Kumar Thatoi P, Tripathy R. Non-Classical monocytes display inflammatory features: Validation in sepsis and systemic lupus erythematous. Sci Rep. 2015;5:13886. doi: 10.1038/srep13886
  125. Chung H, Lee JH, Jo YH, et al. Circulating monocyte counts and its impact on outcomes in patients with severe sepsis including septic shock. Shock . 2019;51(4):423–429. doi: 10.1097/SHK.0000000000001193
  126. Ferreira da Mota NV, Brunialti MK, Santos SS. Immunophenotyping of monocytes during human sepsis shows impairment in antigen presentation. Shock . 2018;50(3):293–300. doi: 10.1097/SHK.0000000000001078
  127. Skrzeczynska J, Kobylarz K, Hartwich Z, Zembala M. CD14 + CD16 + monocytes in the course of sepsis in neonates and small children: monitoring and functional studies. Scand J Immunol. 2002;55:629–638. doi: 10.1046/j.1365-3083.2002.01092.x
  128. Hortová-Kohoutková M, Lázničková P, Bendíčková K, et al. Differences in monocyte subsets are associated with short-term survival in patients with septic shock. J Cell Mol Med. 2020;24(21):12504–1251. doi: 10.1111/jcmm.15791
  129. Lazanovich VA, Markelova EV, Smirnov GA, Pavlov VA. TOLL-receptors on monocytes and their clinical significance in patients with sepsis. Russian Immunological Journal. 2014;8(3(17)):825–828 . EDN: TFFUCD
  130. Lazanovich VA, Markelova EV, Karaulov AV, et al. Clinical significance of TLR2 and TLR4 expression on the cells of the myeloid series and serum cytokine levels in patients with sepsis. Immunopathology, allergology, infectology. 2015;2:71–76. EDN: VAOEDR doi: 10.14427/jipai.2015.2.71
  131. Greco M, Mazzei A, Palumbo C, et al. Flow cytometric analysis of monocytes polarization and reprogramming from inflammatory to immunosuppressive phase during sepsis. EJIFCC . 2019;30(4):371–384.
  132. Ziegler-Heitbrock L. The CD14 + CD16 + blood monocytes: their role ininfection and inflammation. J Leukoc Biol. 2007;81(3):584–592 . doi: 10.1189/jlb.0806510
  133. Belge KU, Dayyani F, Horelt A, Siedlar M. The proinflammatory CD14 + CD16 + DR ++ monocytes are a major source of TNF. J Immunol. 2002;168:3536–3542. doi: 10.4049/jimmunol.168.7.3536
  134. Mizuno K, Toma T, Tsukiji H, et al. Selective expansion of CD16 high CCR2 – subpopulation of circulating monocytes with preferential production of haem oxygenase (HO)-1 in response to acute inflammation. Clin Exp Immunol. 2005;142:461–470. doi: 10.1111/j.1365-2249.2005.02932.x
  135. Kamińska J, Lisowska A, Koper-Lenkiewicz OM, Mikłasz P. Differences in monocyte subsets and monocyte-platelet aggregates in acute myocardial infarction-preliminary results. Am J Med Sci. 2019;357(5):421–434. doi: 10.1016/j.amjms.2019.02.010

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