Inflammatory response and its correction in forming a host response to exposure to adverse environmental factors

Abstract

This study systematically review knowledge about the mechanisms of formation of an inflammatory reaction under the influence of biological, physical, and chemical factors, their similarities and differences, and possible methods of pharmacological correction of pathological conditions associated with excessive activation. The effect of adverse environmental factors, such as biological, physical, and chemical factors, causes a systemic response, which is aimed at maintaining homeostasis and is caused, among other things, by a coordinated reaction of the immune system. Phlogogenic agents result in the activation and regulation of the inflammatory response, which is formed by cellular and humoral components of innate immunity. The activation of innate immunity is characterized by a rapid host response, which diminishes following the elimination of “foreign” invaders, endogenous killer cells, and neogenesis. Depending on the nature of the active factors (biopathogens, allergens, toxins, ionizing radiation, etc.), the mechanisms of immune response arousal have unique features mainly originating from the differences in the recognition of specific molecular patterns and “danger signals” by different receptors. However, inflammatory mediators and inflammatory response patterns at the systemic level are largely similar even under widely different triggers. Inflammation, having evolved as an adaptive reaction directed at the immune response, can lead to the development of chronic inflammation and autoimmune diseases due to a mismatch in mechanisms of its control. A “failure” in the regulation of the inflammatory process is the excessive activation of the immune system, which leads to the cytokine release syndrome (hypercytokinemia, or “cytokine storm”) and can cause self-damage (destruction) of tissues, multiple-organ failure, sepsis, and even death. Modern advances in the study of the pathogenetic bases of the inflammatory response are suggested, such as pharmacological correction using pattern recognition receptor antagonists, pro-inflammatory cytokine inhibitors, or blocking of key control genes or signaling pathways.

Keywords

biopathogens / inflammation / inflammatory reaction / ionizing radiation / new coronavirus infection / adverse environmental factors / toxins / cytokine storm / cytokines

References

[1] Kim JH, Jenrow KA, Brown SL. Mechanisms of radiation-induced normal tissue toxicity and implications for future clinical trials. Radiat Oncol J. 2014;32(3):103–115. DOI: 10.3857/roj.2014.32.3.103

[2] Kim J.H., Jenrow K.A., Brown S.L. Mechanisms of radiation-induced normal tissue toxicity and implications for future clinical trials // Radiat Oncol J. 2014. Vol. 32. Nо. 3. P. 103–115. DOI: 10.3857/roj.2014.32.3.103

[3] Chereshnev VA, Gusev EYu. Immunological and pathophysiological mechanisms of systemic inflammation. Medical Immunology (Russia). 2012;14(1-2):9–20. (In Russ.). DOI: 10.15789/1563-0625-2012-1-2-9-20

[4] Черешнев В.А., Гусев Е.Ю. Иммунологические и патофизиологические механизмы системного воспаления // Медицинская иммунология. 2012. Т. 14, № 1-2. С. 9–20. DOI: 10.15789/1563-0625-2012-1-2-9-20

[5] Chovatiya R, Medzhitov R. Stress, inflammation, and defense of homeostasis. Mol Cell. 2014;54(2):281–288. DOI: 10.1016/j.molcel.2014.03.030

[6] Chovatiya R., Medzhitov R. Stress, inflammation, and defense of homeostasis // Mol Cell. 2014. Vol. 54. Nо. 2. P. 281–288. DOI: 10.1016/j.molcel.2014.03.030

[7] Chen L, Deng H, Cui H, et al. Inflammatory responses and inflammation-associated diseases in organs. Oncotarget. 2018;9(6): 7204–7218. DOI: 10.18632/oncotarget.23208

[8] Chen L., Deng H., Cui H., et al. Inflammatory responses and inflammation-associated diseases in organs // Oncotarget. 2018. Vol. 9. Nо 6. P. 7204–7218. DOI: 10.18632/oncotarget.23208

[9] Medzhitov R. Inflammation 2010: New adventures of an old flame. Cell. 2010;140(6):771–776. DOI:10.1016/j.cell.2010.03.006

[10] Medzhitov R. Inflammation 2010: New adventures of an old flame // Cell. 2010. Vol. 140. Nо. 6. P. 771–776. DOI:10.1016/j.cell.2010.03.006

[11] Litvitsky PF. Inflammation. Current Pediatrics. 2006;5(3):46–51. (In Russ.).

[12] Литвицкий П.Ф. Воспаление // Вопросы современной педиатрии. 2006. Т. 5, № 3. C. 46–51.

[13] Netea MG, Balkwill F, Chonchol M, et al. A guiding map for inflammation. Nat Immunol. 2017;18(8):826–831. DOI: 10.1038/ni.3790

[14] Netea M.G., Balkwill F., Chonchol M., et al. A guiding map for inflammation // Nat Immunol. 2017. Vol. 18. Nо. 8. P. 826–831. DOI: 10.1038/ni.3790

[15] Danyang L, Minghua W. Pattern recognition receptors in health and diseases. Signal Transduct Target Ther. 2021;6(1):291. DOI: 10.1038/s41392-021-00687-0

[16] Danyang L., Minghua W. Pattern recognition receptors in health and diseases // Signal Transduct Target Ther. 2021. Vol. 6. Nо. 1. ID 291. DOI: 10.1038/s41392-021-00687-0

[17] Relja B, Mörs K, Marzi I. Danger signals in trauma. Eur J Trauma Emerg Surg. 2018;44(3):301–316. DOI: 10.1007/s00068-018-0962-3

[18] Relja B., Mörs K., Marzi I. Danger signals in trauma // Eur J Trauma Emerg Surg. 2018. Vol. 44. Nо. 3. P. 301–316. DOI: 10.1007/s00068-018-0962-3

[19] Relja B, Land WG. Damage-associated molecular patterns in trauma. Review Eur J Trauma Emerg Surg. 2020;46(4):751–775. DOI: 10.1007/s00068-019-01235-w

[20] Relja B., Land W.G. Damage-associated molecular patterns in trauma // Review Eur J Trauma Emerg Surg. 2020. Vol. 46. Nо. 4. P. 751–775. DOI: 10.1007/s00068-019-01235-w

[21] Takeuchi O, Akira Sh. Pattern Recognition Receptors and Inflammation. Cell. 2010;140(6):805–820. DOI: 10.1016/j.cell.2010.01.022

[22] Takeuchi O., Akira Sh. Pattern Recognition Receptors and Inflammation // Cell. 2010. Vol. 140. No. 6. P. 805–820. DOI: 10.1016/j.cell.2010.01.022

[23] Barton GM. A calculated response: control of inflammation by the innate immune system. J Clin Invest. 2008;118(2):413–420. DOI: 10.1172/JCI34431

[24] Barton G.M. A calculated response: control of inflammation by the innate immune system // J Clin Invest. 2008. Vol. 118. Nо. 2. P. 413–420. DOI: 10.1172/JCI34431

[25] Garg AD, Galluzzi L, Apetoh L, et al. Molecular and translational classifications of DAMPs in immunogenic cell death. Front Immunol. 2015;6:588. DOI: 10.3389/fimmu.2015.00588

[26] Garg A.D., Galluzzi L., Apetoh L., et al. Molecular and translational classifications of DAMPs in immunogenic cell death // Front Immunol. 2015. Vol. 6. ID 588. DOI: 10.3389/fimmu.2015.00588

[27] Tong A-J, Liu X, Thomas BJ, et al. A stringent systems approach uncovers gene-specific mechanisms regulating inflammation. Cell. 2016;165(1):165–179. DOI: 10.1016/j.cell.2016.01.020

[28] Tong A.-J., Liu X., Thomas B.J., et al. A stringent systems approach uncovers gene-specific mechanisms regulating inflammation // Cell. 2016. Vol. 165. Nо. 1. P. 165–179. DOI: 10.1016/j.cell.2016.01.020

[29] Rivera A, Siracusa MC, Yap GS, Gause WC. Innate cell communication kick-starts pathogen-specific immunity. Nat Immunol. 2016;17(4):356–363. DOI: 10.1038/ni.3375

[30] Rivera A., Siracusa M.C., Yap G.S., Gause W.C. Innate cell communication kick-starts pathogen-specific immunity // Nat Immunol. 2016. Vol. 17. Nо 4. P. 356–363. DOI: 10.1038/ni.3375

[31] Iwasaki A, Medzhitov R. Control of adaptive immunity by the innate immune system. Nat Immunol. 2015;16(4):343–353. DOI: 10.1038/ni.3123

[32] Iwasaki A., Medzhitov R. Control of adaptive immunity by the innate immune system // Nat Immunol. 2015. Vol. 16. No. 4. P. 343–353. DOI: 10.1038/ni.3123

[33] Almeida L, Lochner M, Berod L, Sparwasser T. Metabolic pathways in T cell activation and lineage differentiation. Semin Immunol. 2016;28(5):514–524. DOI: 10.1016/j.smim.2016.10.009

[34] Almeida L., Lochner M., Berod L., Sparwasser T. Metabolic pathways in T cell activation and lineage differentiation // Semin Immunol. 2016. Vol. 28. Nо. 5. P. 514–524. DOI:10.1016/j.smim.2016.10.009

[35] Buck MD, O’Sullivan D, Geltink RIK, et al. Mitochondrial dynamics controls T cell fate through metabolic programming. Cell. 2016;166(1):63–76. DOI: 10.1016/j.cell.2016.05.035

[36] Buck M.D., O’Sullivan D., Geltink R.I.K., et al. Mitochondrial dynamics controls T cell fate through metabolic programming // Cell. 2016. Vol. 166. Nо. 1. P. 63–76. DOI: 10.1016/j.cell.2016.05.035

[37] Goronzy JJ, Weyand CM. Successful and maladaptive T cell aging. Immunity. 2017;46(3):364–378. DOI: 10.1016/j.immuni.2017.03.010

[38] Goronzy J.J., Weyand C.M. Successful and maladaptive T cell aging // Immunity. 2017. Vol. 46. Nо. 3. P. 364–378. DOI: 10.1016/j.immuni.2017.03.010

[39] Ageitos JM, Sánchez-Pérez A, Calo-Mata P, Villa TG. Antimicrobial peptides (AMPs): Ancient compounds that represent novel weapons in the fight against bacteria. Biochem Pharmacol. 2017;133: 117–138. DOI: 10.1016/j.bcp.2016.09.018

[40] Ageitos J.M., Sánchez-Pérez A., Calo-Mata P., Villa T.G. Antimicrobial peptides (AMPs): Ancient compounds that represent novel weapons in the fight against bacteria // Biochem Pharmacol. 2017. Vol. 133. P. 117–138. DOI: 10.1016/j.bcp.2016.09.018

[41] Chairatana Ph, Nolan EM. Defensins, lectins, mucins, and secretory immunoglobulin A: microbe-binding biomolecules that contribute to mucosal immunity in the human gut. Critical Rev Biochem Mol Biol. 2017;52(1):45–56. DOI: 10.1080/10409238.2016.1243654

[42] Chairatana Ph., Nolan E.M. Defensins, lectins, mucins, and secretory immunoglobulin A: microbe-binding biomolecules that contribute to mucosal immunity in the human gut // Critical Rev Biochem Mol Biol. 2017. Vol. 52. Nо. 1. P. 45–56. DOI: 10.1080/10409238.2016.1243654

[43] Moschen AR, Adolph TE, Gerner RR, et al. Lipocalin-2: A master mediator of intestinal and metabolic inflammation. Trends Endocrinol Metabol. 2017;28(5):388–397. DOI: 10.1016/j.tem.2017.01.003

[44] Moschen A.R., Adolph T.E., Gerner R.R., et al. Lipocalin-2: A master mediator of intestinal and metabolic inflammation // Trends Endocrinol Metabol. 2017. Vol. 28. Nо. 5. P. 388–397. DOI: 10.1016/j.tem.2017.01.003

[45] Hajishengallis G, Reis ES, Mastellos DC, et al. Novel mechanisms and functions of complement. Nat Immunol. 2017;18(12):1288–1298. DOI: 10.1038/ni.3858

[46] Hajishengallis G., Reis E.S., Mastellos D.C., et al. Novel mechanisms and functions of complement // Nat Immunol. 2017. Vol. 18. Nо. 12. P. 1288–1298. DOI: 10.1038/ni.3858

[47] Hau CS, Kanda N, Tada Y, et al. Lipocalin-2 exacerbates psoriasiform skin inflammation by augmenting T-helper 17 response. J Dermatol. 2016;43(7):785–794. DOI: 10.1111/1346-8138.13227

[48] Hau C.S., Kanda N., Tada Y., et al. Lipocalin-2 exacerbates psoriasiform skin inflammation by augmenting T-helper 17 response // J Dermatol. 2016. Vol. 43. Nо. 7. P. 785–794. DOI: 10.1111/1346-8138.13227

[49] Bakunina LS, Litvinenko IV, Nakatis YaA, et al. Sepsis: pozhar i bunt na tonushchem v shtorm korable: monografiya. In 3th parts. Part I. Triggery vospaleniya. Retseptsiya triggerov vospaleniya i signal’naya transduktsiya. Pluzhnikov NN, Chepura SV, Khurtsilava OG, editors. Saint-Petersburg: Izd-vo SZGMU im. I.I. Mechnikova; 2018. 232 p. (In Russ.).

[50] Бакунина Л.С., Литвиненко И.В., Накатис Я.А., и др. Сепсис: пожар и бунт на тонущем в шторм корабле: монография. В 3 частях. Часть I. Триггеры воспаления. Рецепция триггеров воспаления и сигнальная трансдукция / под ред. Н.Н. Плужникова, С.В. Чепура, О.Г. Хурцилава. Санкт-Петербург: Изд-во СЗГМУ им. И.И. Мечникова, 2018. 232 с.

[51] Longo DL, Fajgenbaum DC, June CH. Cytokine Storm. N Engl J Med. 2020;383(23):2255–2273. DOI: 10.1056/NEJMra2026131

[52] Longo D.L., Fajgenbaum D.C., June C.H. Cytokine Storm // N Engl J Med. 2020. Vol. 383. Nо. 23. P. 2255–2273. DOI: 10.1056/NEJMra2026131

[53] Tisoncik JR, Korth MJ, Simmons CP, et al. Into the Eye of the Cytokine Storm. Microbiol Mol Biol Rev. 2012;76(1):16–32. DOI: 10.1128/MMBR.05015-11

[54] Tisoncik J.R., Korth M.J., Simmons C.P., et al. Into the Eye of the Cytokine Storm // Microbiol Mol Biol Rev. 2012. Vol. 76. Nо. 1. P. 16–32. DOI: 10.1128/MMBR.05015-11

[55] Lee DW, Gardner R, Porter DL, et al. Current concepts in the diagnosis and management of cytokine release syndrome. Blood. 2014;124(2):188–195. DOI: 10.1182/blood-2014-05-552729

[56] Lee D.W., Gardner R., Porter D.L., et al. Current concepts in the diagnosis and management of cytokine release syndrome // Blood. 2014. Vol. 124. Nо. 2. P. 188–195. DOI: 10.1182/blood-2014-05-552729

[57] Shimabukuro-Vornhagen A, Gödel Ph, Subklewe M, et al. Cytokine release syndrome. J Immunother Cancer. 2018;6(1):56. DOI: 10.1186/s40425-018-0343-9

[58] Shimabukuro-Vornhagen A., Gödel Ph., Subklewe M., et al. Cytokine release syndrome // J Immunother Cancer. 2018. Vol. 6. No. 1. P. 56. DOI: 10.1186/s40425-018-0343-9

[59] Wong JP, Viswanathan S, Wang M. Current and future developments in the treatment of virus-induced hypercytokinemia. Future Med Chem. 2017;9(2):169–178. DOI: 10.4155/fmc-2016-0181

[60] Wong J.P., Viswanathan S., Wang M. Current and future developments in the treatment of virus-induced hypercytokinemia // Future Med Chem. 2017. Vol. 9. Nо. 2. P. 169–178. DOI: 10.4155/fmc-2016-0181

[61] Ye Q, Wang B, Mao J. The pathogenesis and treatment of the `Cytokine Storm’ in COVID-19. J Infect. 2020;80(6):607–613. DOI: 10.1016/j.jinf.2020.03.037

[62] Ye Q., Wang B., Mao J. The pathogenesis and treatment of the 'Cytokine Storm' in COVID-19 // J Infect. 2020. Vol. 80. Nо. 6. P. 607–613. DOI: 10.1016/j.jinf.2020.03.037

[63] Soy M, Keser G, Atagündüz P. Pathogenesis and treatment of cytokine storm in COVID-19. Turk J Biol. 2021;45(4):372–389. DOI: 10.3906/biy-2105-37

[64] Soy M., Keser G., Atagündüz P. Pathogenesis and treatment of cytokine storm in COVID-19 // Turk J Biol. 2021. Vol. 45. Nо. 4. P. 372–389. DOI: 10.3906/biy-2105-37

[65] Kim JS, Lee JY, Yang JW, et al. Immunopathogenesis and treatment of cytokine storm in COVID-19. Theranostics. 2021;11(1): 316–329. DOI: 10.7150/thno.49713

[66] Kim J.S., Lee J.Y., Yang J.W., et al. Immunopathogenesis and treatment of cytokine storm in COVID-19 // Theranostics. 2021. Vol. 11. Nо. 1. P. 316–329. DOI: 10.7150/thno.49713

[67] Barker ChA, Kim SK, Budhu S, et al. Cytokine release syndrome after radiation therapy: case report and review of the literature. J Immunother Cancer. 2018;6(1):1. DOI: 10.1186/s40425-017-0311-9

[68] Barker Ch.A., Kim S.K., Budhu S., et al. Cytokine release syndrome after radiation therapy: case report and review of the literature // J Immunother Cancer. 2018. Vol. 6. No. 1. ID 1. DOI: 10.1186/s40425-017-0311-9

[69] Zhang Ch, Liang Zh, Ma Sh, et al. Radiotherapy and Cytokine Storm: Risk and Mechanism. Front Oncol. 2021;11:670464. DOI: 10.3389/fonc.2021.670464

[70] Zhang Ch., Liang Zh., Ma Sh., et al. Radiotherapy and Cytokine Storm: Risk and Mechanism // Front Oncol. 2021. Vol. 11. ID 670464. DOI: 10.3389/fonc.2021.670464

[71] Mukherjee D, Coates PhJ, Lorimore SA, Wright EG. Responses to ionizing radiation mediated by inflammatory mechanisms. J Pathol. 2014;232(3):289–299. DOI: 10.1002/path.4299

[72] Mukherjee D., Coates Ph.J., Lorimore S.A., Wright E.G. Responses to ionizing radiation mediated by inflammatory mechanisms // J Pathol. 2014. Vol. 232. Nо. 3. Р. 289–299. DOI: 10.1002/path.4299

[73] Schaue D, Micewicz ED, Ratikan JA, et al. Radiation and Inflammation. Semin Radiat Oncol. 2015;25(1):4–10. DOI: 10.1016/j.semradonc.2014.07.007

[74] Schaue D., Micewicz E.D., Ratikan J.A., et al. Radiation and Inflammation // Semin Radiat Oncol. 2015. Vol. 25. Nо. 1. Р. 4–10. DOI: 10.1016/j.semradonc.2014.07.007

[75] Yahyapour R, Amini P, Rezapour S, et al. Radiation-induced inflammation and autoimmune diseases. Mil Med Res. 2018;5:9. DOI: 10.1186/s40779-018-0156-7

[76] Yahyapour R., Amini P., Rezapour S., et al. Radiation-induced inflammation and autoimmune diseases // Mil Med Res. 2018. Vol. 5. ID 9. DOI: 10.1186/s40779-018-0156-7

[77] Rios CI, Cassatt DR, Hollingsworth BA, et al. Commonalities between COVID-19 and radiation injury. Radiat Res. 2021;195(1): 1–24. DOI: 10.1667/RADE-20-00188.1

[78] Rios C.I., Cassatt D.R., Hollingsworth B.A., et al. Commonalities between COVID-19 and radiation injury // Radiat Res. 2021. Vol. 195. Nо. 1. P. 1–24. DOI: 10.1667/RADE-20-00188.1

[79] Gorbunov NV, Sharma P. Protracted oxidative alterations in the mechanism of hematopoietic acute radiation syndrome. Antioxidants (Basel). 2015;4(1):134–152. DOI: 10.3390/antiox4010134

[80] Gorbunov N.V., Sharma P. Protracted oxidative alterations in the mechanism of hematopoietic acute radiation syndrome // Antioxidants (Basel). 2015. Vol. 4. Nо. 1. P. 134–152. DOI: 10.3390/antiox4010134

[81] Adjemian S, Oltean T, Martens S, et al. Ionizing radiation results in a mixture of cellular outcomes including mitotic catastrophe, senescence, methuosis, and iron-dependent cell death. Cell Death Dis. 2020;11(11):1003. DOI: 10.1038/s41419-020-03209-y

[82] Adjemian S., Oltean T., Martens S., et al. Ionizing radiation results in a mixture of cellular outcomes including mitotic catastrophe, senescence, methuosis, and iron-dependent cell death // Cell Death Dis. 2020. Vol. 11. Nо. 11. ID 1003. DOI: 10.1038/s41419-020-03209-y

[83] Chen Y, Li Y, Huang L, et al. Antioxidative stress: inhibiting reactive oxygen species production as a cause of radioresistance and chemoresistance. Oxid Med Cell Longev. 2021;8:6620306. DOI: 10.1155/2021/6620306

[84] Chen Y., Li Y., Huang L., et al. Antioxidative stress: inhibiting reactive oxygen species production as a cause of radioresistance and chemoresistance // Oxid Med Cell Longev. 2021. Vol. 8. ID 6620306. DOI: 10.1155/2021/6620306

[85] Jandhyala DM, Wong J, Mantis NJ, et al. A novel zak knockout mouse with a defective ribotoxic stress response. Toxins (Basel). 2016;8(9):259. DOI: 10.3390/toxins8090259

[86] Jandhyala D.M., Wong J., Mantis N.J., et al. A novel zak knockout mouse with a defective ribotoxic stress response // Toxins (Basel). 2016. Vol. 8. Nо. 9. ID 259. DOI: 10.3390/toxins8090259

[87] Wong J, Magun BE, Wood LJ. Lung inflammation caused by inhaled toxicants: a review. Int J Chron Obstruct Pulmon Dis. 2016;11(1):1391–1401. DOI: 10.2147/COPD.S106009

[88] Wong J., Magun B.E., Wood L.J. Lung inflammation caused by inhaled toxicants: a review // Int J Chron Obstruct Pulmon Dis. 2016. Vol. 11. No. 1. P. 1391–1401. DOI: 10.2147/COPD.S106009

[89] Lindauer ML, Wong J, Iwakura Y, Magun BE. Pulmonary inflammation triggered by ricin toxin requires macrophages and IL-1 signaling. J Immunol. 2009;183(2):1419–1426. DOI: 10.4049/jimmunol.0901119

[90] Lindauer M.L., Wong J., Iwakura Y., Magun B.E. Pulmonary inflammation triggered by ricin toxin requires macrophages and IL-1 signaling // J Immunol. 2009. Vol. 183. Nо. 2. P. 1419–1426. DOI: 10.4049/jimmunol.0901119

[91] Dong M, Yu H, Wang Y, et al. Critical role of toll-like receptor 4 (TLR4) in ricin toxin-induced inflammatory responses in macrophages. Toxicol Lett. 2020;321:54–60. DOI: 10.1016/j.toxlet.2019.12.021

[92] Dong M., Yu H., Wang Y., et al. Critical role of toll-like receptor 4 (TLR4) in ricin toxin-induced inflammatory responses in macrophages // Toxicol Lett. 2020. Vol. 321. P. 54–60. DOI: 10.1016/j.toxlet.2019.12.021

[93] Xu N, Yu K, Yu H, et al. Recombinant ricin toxin binding subunit B (RTB) stimulates production of TNF-α by mouse macrophages through activation of TLR4 signaling pathway. Front Pharmacol. 2020;11:526129. DOI: 10.3389/fphar.2020.526129

[94] Xu N., Yu K., Yu H., et al. Recombinant ricin toxin binding subunit B (RTB) stimulates production of TNF-α by mouse macrophages through activation of TLR4 signaling pathway // Front Pharmacol. 2020. Vol. 11. ID 526129. DOI: 10.3389/fphar.2020.526129

[95] Chikuma Sh. CTLA-4, an essential immune-checkpoint for Tcell activation. Curr Top Microbiol Immunol. 2017;410:99–126. DOI: 10.1007/82_2017_61

[96] Chikuma Sh. CTLA-4, an essential immune-checkpoint for Tcell activation // Curr Top Microbiol Immunol. 2017. Vol. 410. P. 99–126. DOI: 10.1007/82_2017_61

[97] Dimeloe S, Mehling M, Frick C, et al. The immune-metabolic basis of effector memory CD4+ Tcell function under hypoxic conditions. J Immunol. 2016;196(1):106–114. DOI: 10.4049/jimmunol.1501766

[98] Dimeloe S., Mehling M., Frick C., et al. The immune-metabolic basis of effector memory CD4+ Tcell function under hypoxic conditions // J Immunol. 2016. Vol. 196. Nо. 1. P. 106–114. DOI: 10.4049/jimmunol.1501766

[99] Liu Q, Zhou Y, Yang Zh. The cytokine storm of severe influenza and development of immunomodulatory therapy. Cell Mol Immunol. 2016;13(1):3–10. DOI: 10.1038/cmi.2015.74

[100] Liu Q., Zhou Y., Yang Zh. The cytokine storm of severe influenza and development of immunomodulatory therapy // Cell Mol Immunol. 2016. Vol. 13. Nо. 1. P. 3–10. DOI: 10.1038/cmi.2015.74

[101] Zhang W, Zhao Y, Zhang F, et al. The use of anti-inflammatory drugs in the treatment of people with severe coronavirus disease 2019 (COVID-19): The Perspectives of clinical immunologists from China. Clin Immunol. 2020;214:108393. DOI: 10.1016/j.clim.2020.108393

[102] Zhang W., Zhao Y., Zhang F., et al. The use of anti-inflammatory drugs in the treatment of people with severe coronavirus disease 2019 (COVID-19): The Perspectives of clinical immunologists from China // Clin Immunol. 2020. Vol. 214. ID 108393. DOI: 10.1016/j.clim.2020.108393

[103] Cavalli G, Dinarello ChA. Anakinra therapy for non-cancer inflammatory diseases. Front Pharmacol. 2018;9:1157. DOI: 10.3389/fphar.2018.01157

[104] Cavalli G., Dinarello Ch.A. Anakinra therapy for non-cancer inflammatory diseases // Front Pharmacol. 2018. Vol. 9. ID 1157. DOI: 10.3389/fphar.2018.01157

[105] Dinarello ChA. Treatment of inflammatory diseases with IL-1 blockade. Curr Otorhinolaryngol Rep. 2018;6(1):1–14. DOI: 10.1007/s40136-018-0181-9

[106] Dinarello Ch.A. Treatment of inflammatory diseases with IL-1 blockade // Curr Otorhinolaryngol Rep. 2018. Vol. 6. Nо. 1. P. 1–14. DOI: 10.1007/s40136-018-0181-9

[107] Christersdottir T, Pirault J, Gisterå A, et al. Prevention of radiotherapy-induced arterial inflammation by interleukin-1 blockade. Eur Heart J. 2019;40(30):2495–2503. DOI: 10.1093/eurheartj/ehz206

[108] Christersdottir T., Pirault J., Gisterå A., et al. Prevention of radiotherapy-induced arterial inflammation by interleukin-1 blockade // Eur Heart J. 2019. Vol. 40. Nо. 30. P. 2495–2503. DOI: 10.1093/eurheartj/ehz206

[109] Gao W, Xiong Y, Li Q, Yang H. Inhibition of Toll-like receptor signaling as a promising therapy for inflammatory diseases: A journey from molecular to nano therapeutics. Front Physiol. 2017;8:508. DOI: 10.3389/fphys.2017.00508

[110] Gao W., Xiong Y., Li Q., Yang H. Inhibition of Toll-like receptor signaling as a promising therapy for inflammatory diseases: A journey from molecular to nano therapeutics // Front Physiol. 2017. Vol. 8. ID 508. DOI: 10.3389/fphys.2017.00508

[111] Obinata H, Hla T. Sphingosine 1-phosphate and inflammation. Int Immunol. 2019;31(9):617–625. DOI: 10.1093/intimm/dxz037

[112] Obinata H., Hla T. Sphingosine 1-phosphate and inflammation // Int Immunol. 2019. Vol. 31. Nо. 9. P. 617–625. DOI: 10.1093/intimm/dxz037

[113] Marsolais D, Hahm B, Kevin B, et al. A critical role for the sphingosine analog AAL-R in dampening the cytokine response during influenza virus infection. Proc Natl Acad Sci USA. 2009;106(5): 1560–1565. DOI: 10.1073/pnas.0812689106

[114] Marsolais D., Hahm B., Kevin B., et al. A critical role for the sphingosine analog AAL-R in dampening the cytokine response during influenza virus infection // Proc Natl Acad Sci USA. 2009. Vol. 106. Nо. 5. P. 1560–1565. DOI: 10.1073/pnas.0812689106

[115] Walsh KB, Teijaro JR, Wilker PR, et al. Suppression of cytokine storm with a sphingosine analog provides protection against pathogenic influenza virus. Proc Natl Acad Sci USA. 2011;108(29):12018–12023. DOI: 10.1073/pnas.1107024108

[116] Walsh K.B, Teijaro J.R., Wilker P.R., et al. Suppression of cytokine storm with a sphingosine analog provides protection against pathogenic influenza virus // Proc Natl Acad Sci USA. 2011. Vol. 108. Nо. 29. P. 12018–12023. DOI: 10.1073/pnas.1107024108

[117] Teijaro JR, Walsh KB, Rice S, et al. Mapping the innate signaling cascade essential for cytokine storm during influenza virus infection. Proc Natl Acad Sci USA. 2014;111(10):3799–3804. DOI: 10.1073/pnas.1400593111

[118] Teijaro J.R., Walsh K.B., Rice S., et al. Mapping the innate signaling cascade essential for cytokine storm during influenza virus infection // Proc Natl Acad Sci USA. 2014. Vol. 111. Nо. 10. P. 3799–3804. DOI: 10.1073/pnas.1400593111

[119] Jacobson JR. Sphingolipids as a novel therapeutic target in radiation-induced lung injury. Cell Biochem Biophys. 2021;79(3): 509–516. DOI: 10.1007/s12013-021-01022-8

[120] Jacobson J.R. Sphingolipids as a novel therapeutic target in radiation-induced lung injury // Cell Biochem Biophys. 2021. Vol. 79. Nо. 3. P. 509–516. DOI: 10.1007/s12013-021-01022-8

[121] Naz1 F, Arish M. Battling COVID-19 Pandemic: Sphingosine-1-Phosphate Analogs as an Adjunctive Therapy? Front Immunol. 2020;11:1102. DOI: 10.3389/fimmu.2020.01102

[122] Naz1 F., Arish M. Battling COVID-19 Pandemic: Sphingosine-1-Phosphate Analogs as an Adjunctive Therapy? // Front Immunol. 2020. Vol. 11. ID 1102. DOI: 10.3389/fimmu.2020.01102

[123] Tasat DR, Yakisich JS. Rationale for the use of sphingosine analogues in COVID-19 patients. Clin Med (Lond). 2021;21(1): e84–e87. DOI: 10.7861/clinmed.2020-0309

[124] Tasat D.R., Yakisich J.S. Rationale for the use of sphingosine analogues in COVID-19 patients // Clin Med (Lond). 2021. Vol. 21. Nо. 1. P. e84–e87. DOI: 10.7861/clinmed.2020-0309

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