Abstract:Patients with leprosy varies in the degree of cellular immune defect,but the mechanism remains unclear. Macrophages,a group of immunocytes with different phenotypes and functions,are important cell components in the immune response,and participate in the occurrence and development of leprosy. The polarization of macrophages phenotypes is regulated by many factors. In tuberculoid leprosy,macrophages are polarized into M1 phenotype;in lepromatous leprosy,macrophages are polarized into M2 phenotype. We reviewed the research about the effects of macrophage in the pathogenic mechanism of leprosy infection,so as to provide a theoretical basis for leprosy prevention and treatment.
王涧, 严丽英, 徐新美, 刘干红,沈惠良. 巨噬细胞在麻风免疫致病机制中的作用[J]. 预防医学, 2020, 32(5): 475-478.
WANG Jian, YAN Liying, XU Xinmei, LIU Ganhong, SHEN Huiliang. Study progress on macrophages in the immunological pathogenesis of leprosy. Preventive Medicine, 2020, 32(5): 475-478.
NATH I, SAINI C, VALLURI V L.Immunology of leprosy anddiagnostic challenges[J].Clin Dermatol,2015,33(1):90-98.
[2]
DE ALMEIDA-NETO F B, ASSIS COSTA V M, OLIVEIRA-FILHO A F, et al. TH17 cells, interleukin-17 and interferon-γin patients and households contacts of leprosy with multibacillary and paucibacillary forms before and after the start of chemotherapy treatment[J]. J Eur Acad Dermatol Venereol, 2015, 29(7): 1354-1361.
FONSECA A B, SIMON M D, CAZZANIGA R A, et al. The influence of innate and adaptative immune responses on the differential clinical outcomes of leprosy[J/OL]. Infect Dis Poverty (2017-02-06)[2019-12-30]. https://www.ncbi.nlm.nih.gov/pubmed?term=the%20influence%20of%20innate%20and%20adaptive%20immune%20responses%20on%20the%20differential%20clinical%20outcomes%20of%20leprosy&cmd=correctspelling. DOI:10.1186/s40249-016-0229-3.
[8]
PINHEIRO R O,SCHMITZ V,SILVA B J A,et al. Innate immune responses in leprosy[J/OL]. Front Immunol (2018-03-28)[2019-12-30]. https://www.ncbi.nlm.nih.gov/pubmed/29643852.DOI:10.3389/fimmu.2018.00518.
[9]
赵辩. 中国临床皮肤病学[M].南京:江苏科学技术出版社,2010:467-484.
[10]
LASTRIA J C,ABREU M A. Leprosy: review of the epidemiological, clinical, and etiopathogenic aspects-part 1[J]. An Bras Dermatol,2014,89(2): 205-218.
[11]
TALHARI C, TALHARI S, PENNA G O.Clinical aspects of leprosy[J].Clin Dermatol,2015,33(1): 26-37.
[12]
SILVA C A, DANELISHVILI L, MCNAMARA M, et al.Interaction of Mycobacterium leprae with human airway epithelial cells: adherence, entry, survival, and identification of potential adhesins by surface proteome analysis[J].Infect Immun, 2013, 81(7): 2645-2659.
[13]
ARAUJO S, LOBATO J, REIS E D E M, et al. Unveiling healthy carriers and subclinical infections among household contacts of leprosy patients who play potential roles in the disease chain of transmission[J]. Mem Inst Oswaldo Cruz,2012,107(Suppl.1): 55-59.
[14]
DE LIMA C S, MARQUES M A, DEBRIE A S, et al. Heparin-binding hemagglutinin (HBHA) of Mycobacterium leprae is expressed during infection and enhances bacterial adherence to epithelial cells[J]. FEMS Microbiol Lett,2009,292(2): 162-169.
[15]
FUKUI S, LWAMOTO N, TAKATANI A, et al.M1 and M2 monocytes in rheumatoid arthritis: a contribution of imbalance of M1/M2 monocytes to osteoclastogenesis[J/OL]. Front Immunol,2018,8 [2019-12-30]. https://doi.org/10.3389/fimmu.2017.01958.
[16]
WANG L X, ZHANG S X, WU H J, et al.M2b macrophage polarization and its roles in diseases[J]. J Leukoc Biol, 2019, 106(2): 345-358.
[17]
KLEINNIJENHUIS J, OOSTING M, JOOSTEN L A, et al.Innate immune recognition of Mycobacterium tuberculosis[J/OL].Clin Dev Immunol,2011 (2011-01-29)[2019-12-30].http://dx.doi.org/10.1155/2011/405310.
[18]
DE SOUSA J R, LUCENA NETD F D, SOTTO M N, et al. Immunohistochemical characterization of the M4 macrophage population in leprosy skin lesions[J/OL]. BMC Infect Dis,2018,18 (2018-11-15)[2019-12-30].https://doi.org/10.1186/s12879-018-3478-x.
[19]
FACHIN L R, SOARES C T, BELONE A F, et al.Immunohistochemical assessment of cell populations in leprosy-spectrum lesions and reactional forms[J]. Histol Histopathol,2017,32(4): 385-396.
[20]
DE SOUSA J R, DE SOUSA R P, AÃRAO T L, et al. In situ expression of M2 macrophage subpopulation in leprosy skin lesions[J].Acta Trop,2016,157: 108-114.
[21]
MARTINEZ F O,GORDON S,LOCATI M,et al.Transcriptional profiling of the human monocyte-to-macrophage differentiation and polarization: new molecules and patterns of gene expression[J]. J Immunol,2006,177(10): 7303-7311.
[22]
GAO H,HUANG F Y,WANG Z P.Research trends of macrophage polarization: a bibliometric analysis[J].Chin Med J (Engl.) 2018,131(24): 2968-2975.
[23]
HUANG Z, LUO Q, GUO Y, et al. Mycobacterium tuberculosis-induced polarization of human macrophage orchestrates the formation and development of tuberculous granulomas in vitro[J/OL]. PLoS One,2015,10 (6) [2019-12-30]. https://doi.org/10.1371/journal.pone.0129744.
[24]
WANG Z C, YAO Y, WANG N, et al.Deficiency in interleukin-10 production by M2 macrophages in teosinophilic chronic rhinosinusitis with nasal polyps[J]. Int Forum Allergy Rhinol,2018,8(11): 1323-1333.
KIBBIE J, TELES R M, WANG Z, et al. Jagged1 instructs macrophage differentiation in leprosy[J/OL]. PLoS Pathogens, 2016,12(8) [2019-12-30]. https://doi.org/10.1371/journal.ppat.1005808.
MOURA D F, DE MATTOS K A, AMADEU T P, et al. CD163 favors Mycobacterium leprae survival and persistence by promoting anti-inflammatory pathways in lepromatous macrophages[J].Eur J Immunol,2012,42(11): 2925-2936.
[33]
UPADHYAY R, DUA B, SHARMA B, et al.Transcription factors STAT-4, STAT-6 and CREB regulate Th1/Th2 response in leprosy patients: effect of M. leprae antigens[J]. BMC Infect Dis,2019,19(1): 1-11.