Peranan Sel Sistem Imun Alamiah Pada Infeksi Mycobacterium tuberculosis

Chandra Wijaya, Fatmawati Fatmawati

Abstract

Mycobacterium tuberculosis infection which causes tuberculosis is still a major health problem worldwide due to high morbidity and mortality, where in 2018 tuberculosis caused 1.5 million deaths. The degree of pulmonary tuberculosis varies from mild infiltration, chronic infection, cavity formation to severe and destructive tuberculosis. The difference in the degree of pulmonary tuberculosis is influenced by the response of the immune system to M. tuberculosis. When M. tuberculosis infects the lungs, the human immune system will carry out a series of processes to limit the spread and replication of bacteria. The immune system against M. tuberculosis consists of an innate immune system involving cellular components such as macrophages, neutrophils, Natural Killer (NK cells), dendritic cells and upper respiratory epithelium and an acquired immune response which is mainly mediated by T lymphocyte cells of host that is responsible for recognizing and controlling invasion by pathogens. This review will describe the role of natural immune system cells in M. tuberculosis infection. In addition, a complete description of M. tuberculosis infection will also be discussed to increase understanding of the role of natural immune system cells in M. tuberculosis infection.

Keywords

cellular immune response, innate immune response, Mycobacterium tuberculosis, tuberculosis

References

WHO. Global Tuberculosis Report. 2018. Available online at: http://www. who.int/tb/publications/global_report/en/

Jee B. Understanding the early host immune response against Mycobacterium tuberculosis. Centr Eur J Immunol 2020; 45 (1): 99-103

Zuniga J, Torres-Garcıa D, Santos-Mendoza T, Rodriguez-Reyna TS, Granados J, Yunis EJ. Cellular and Humoral Mechanisms Involved in the Control of Tuberculosis. Clinical and Developmental Immunology Volume 2012, Article ID 193923, 18 pages doi:10.1155/2012/193923

De Martino M, Lodi L, Galli L and Chiappini E. 2019. Immune Response to Mycobacterium tuberculosis: A Narrative Review. Front. Pediatr. 7:350. doi: 10.3389/fped.2019.00350

Bermudez, L.E.; Goodman, J. Mycobacterium tuberculosis invades and replicates within type II alveolar cells. Infect. Immun. 1996, 64, 1400–1406.

Li Y, Wang Y, Liu X. The role of airway epithelial cells in response to mycobacteria infection. Clin Dev Immunol. 2012:791392. doi: 10.1155/2012/791392

Harriff MJ, Cansler ME, Toren KG, Canfield ET, Kwak S, Gold MC, et al. 2014. Human lung epithelial cells contain Mycobacterium tuberculosis in a late endosomal vacuole and are efficiently recognized by CD8+ T cells. PLoS ONE. 9: e97515. doi: 10.1371/journal.pone.0097515

Echeverria-Valencia G, Flores-Villalva S.; Espitia CI. Virulence Factors and Pathogenicity of Mycobacterium. In Mycobacterium-Research and Development; Tech: Rijeka, Croatia, 2018; pp. 231–255.

Sia JK, Georgieva M, Rengarajan J. 2015. Innate Immune Defenses in Human Tuberculosis: An Overview of the Interactions between Mycobacterium tuberculosis and Innate Immune Cells. Journal of Immunology Research Volume 2015, Article ID 747543, 12 pages http://dx.doi.org/10.1155/2015/747543

Philips JA, Ernst JD. 2011. Tuberculosis pathogenesis and immunity. Annual Review of Pathology: Mechanisms of Disease, Vol. 7, pp. 353–384

Kleinnijenhuis J, Oosting M, Joosten LAB, Netea MG, Crevel MV. Innate Immune Recognition of Mycobacterium tuberculosis. Clinical and Developmental Immunology Volume 2011, Article ID 405310, 12 pages doi:10.1155/2011/405310

Liu CH, Liu H, Ge B. 2017. Innate immunity in tuberculosis: host defense vs pathogen evasion. Cellular & Molecular Immunology 14 :963–975

Lee J, Hartman M, Kornfeld H. 2009. Macrophage apoptosis in tuberculosis. Yonsei Med J 50: 1–11

Van de Veerdonk FL, Teirlinck AC, Kleinnijenhuis J, Kullberg BJ, van Crevel R, van der Meer JW, Joosten LA, Netea MG. 2010. Mycobacterium tuberculosis induces IL-17A responses through TLR4 and dectin-1 and is critically dependent on endogenous IL-1. J Leukoc Biol 88:227-32.

LimYJ, Yi MH, Choi JA, Lee J, Han JY, Jo SH. Roles of endoplasmic reticulum stress-mediated apoptosis in M1-polarized macrophages during mycobacterial infections. Sci. Rep. 2016, 6, 37211.

Mills, C.D. M1 and M2 macrophages: Oracles of health and disease. Crit. Rev. Immunol. 2012, 32, 463–488.

Bloom BR, “Pathogenesis of pulmonary tuberculosis,” in An Interplay between Tissue-Damaging and Macrophage Activating Immune Responses: Dual Mechanisms That Control Bacillary Multiplication, B. R. Bloom, Ed., pp. 459–484, American Society for Microbiology, Washington, DC, USA, 1994.

Ernst JD. Macrophage receptors for Mycobacterium tuberculosis. Infect Immun. 1998 Apr;66(4):1277-81. doi: 10.1128/IAI.66.4.1277-1281.1998. PMID: 9529042; PMCID: PMC108049.

Zhang Y, Zhou Y, Lou J, Li J, Bo L, Zhu K, et al. PD-L1 blockade improves survival in experimental sepsis by inhibiting lymphocyte apoptosis and reversing monocyte dysfunction. Crit Care. (2010) 14:R220.doi: 10.1186/cc935

Nandi B, Behar SM. Regulation of neutrophils by interferon-gamma limits lung inflammation during tuberculosis infection. J. Exp. Med. 2011, 208, 2251–2259.

Barrios-Payán J, Aguilar-León D, Lascurain-Ledezma R, Hernández-Pando R. Neutrophil participation in early control and immune activation during experimental pulmonary tuberculosis. Gac. Med. Mex. 2006, 142, 273–281.

Pokkali S, Rajavelu P, Sudhakar R, Das SD. Phenotypic modulation in Mycobacterium tuberculosis infected neutrophil during tuberculosis. Indian J. Med. Res. 2009, 130, 185–192

McCracken JM, Allen LA. 2014. Regulation of human neutrophil apoptosis and lifespan in health and disease. J. Cell Death, 7 : 15–23

Arora P, Foster EL, Porcelli SA. CD1d and natural killer T cells in immunity to Mycobacterium tuberculosis. Adv Exp Med Biol. (2013) 783:199–223. doi: 10.1007/978-1-4614-6111-1_11

Khan N, Vidyarthi A, Pahari S, Agrewala JN.2016. Distinct strategies employed by dendritic cells and macrophages in restricting Mycobacterium tuberculosis infection: different philosophies but same desire. Int Rev Immunol. 35:386–98. doi: 10.3109/08830185.2015.1015718

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