Advances in application of Jurkat cell model in research on infectious diseases

CHEN Jing-Lun; NONG Guang-Min

doi:10.7499/j.issn.1008-8830.2018.03.014

PDF(919 KB)

Chinese Journal of Contemporary Pediatrics ›› 2018, Vol. 20 ›› Issue (3) : 236-242. DOI: 10.7499/j.issn.1008-8830.2018.03.014

REVIEW

Advances in application of Jurkat cell model in research on infectious diseases

CHEN Jing-Lun, NONG Guang-Min

Author information +

History +

Abstract

Infectious diseases can be caused by multiple pathogens, which can produce specific immune response in human body. The immune response produced by T cells is cellular immunity, which plays an important role in the anti-infection process of human body, and can participate in immunological protection and cause immunopathology. The outcome of various infectious diseases is closely related to cellular immune function, especially the function of T cells. Jurkat cells belong to the human acute T lymphocyte leukemia cell line. Jurkat cell model can simulate the function T lymphocytes, so it is widely used in the in vitro studies of T cell signal transduction, cytokines, and receptor expression, and can provide reference and guidance for the treatment of various infectious diseases and the research on their pathogenesis. The Jurkat cell model has been widely used in the in vitro studies of viral diseases and atypical pathogens, but parasitic infection studies using the Jurkat cell model are still rare. This article reviews advances in the application of Jurkat cell model in the research on infectious diseases.

Key words

Jurkat cell / T cell / Cell model / Infectious disease

Cite this article

EndNote

Ris (Procite)

Bibtex

Download Citations

CHEN Jing-Lun, NONG Guang-Min. Advances in application of Jurkat cell model in research on infectious diseases[J]. Chinese Journal of Contemporary Pediatrics. 2018, 20(3): 236-242 https://doi.org/10.7499/j.issn.1008-8830.2018.03.014

References

[1] Wang X, Zhao J, Tang S, et al. c-FLIPL regulates PKC via AP-2 to inhibit Bax-mediated apoptosis induced by HIV-1 gp120 in Jurkat cells[J]. Mol Cell Biochem, 2009, 330(1-2):23-29.
[2] Tan J, Wang X, Devadas K, et al. Some mechanisms of FLIP expression in inhibition of HIV-1 replication in Jurkat cells, CD4⁺ T cells and PBMCs[J]. J Cell Physiol, 2013, 228(12):2305-2313.
[3] Wang X, Viswanath R, Zhao J, et al. Changes in the level of apoptosis-related proteins in Jurkat cells infected with HIV-1 versus HIV-2[J]. Mol Cell Biochem, 2010, 337(1-2):175-183.
[4] Torresilla C, Carmo SD, Larocque E, et al. The antisense protein of HTLV-2 positively modulates HIV-1 replication[J]. Retrovirology, 2014, 11(Suppl 1):118.
[5] Wang X, Tan J, Zhao J, et al. Some findings of FADD knockdown in inhibition of HIV-1 replication in Jurkat cells and PBMCs[J]. Mol Cell Biochem, 2014, 393(1-2):181-190.
[6] Wang X, Tan J, Biswas S, et al. Pandemic influenza A (H1N1) virus infection increases apoptosis and HIV-1 replication in HIV-1 infected Jurkat cells[J]. Viruses, 2016, 8(2). pii:E33.
[7] Ren XX, Ma L, Sun WW, et al. Dendritic cells maturated by co-culturing with HIV-1 latently infected Jurkat T cells or stimulating with AIDS-associated pathogens secrete TNF-α to reactivate HIV-1 from latency[J]. Virulence, 2017, 8(8):1732-1743.
[8] Lu P, Qu X, Shen Y, et al. The BET inhibitor OTX015 reactivates latent HIV-1 through P-TEFb[J]. Sci Rep, 2016, 6:24100.
[9] Dahabieh MS, Ooms M, Brumme C, et al. Direct non-productive HIV-1 infection in a T-cell line is driven by cellular activation state and NFκB[J]. Retrovirology, 2014, 11:17.
[10] Wang X, Mbondji-Wonje C, Zhao J, et al. IL-1β and IL-18 inhibition of HIV-1 replication in Jurkat cells and PBMCs[J]. Biochem Biophys Res Commun, 2016, 473(4):926-930.
[11] Adeyanju K, Dekaban GA, Rieder MJ. Cytoplasmic distribution of HIV-1 tat sensitizes Jurkat T cells to sulphamethoxazole-hydroxylamine induced toxicity[J]. HIV Curr Res, 2016, 1(1):1000105.
[12] Amet T, Lan J, Shepherd N, et al. Glycosylphosphatidylinositol anchor deficiency attenuates the production of infectious HIV-1 and renders virions sensitive to complement attack[J]. AIDS Res Hum Retroviruses, 2016, 32(10-11):1100-1112.
[13] Do T, Murphy G, Earl LA, et al. Three-dimensional imaging of HIV-1 virological synapses reveals membrane architectures involved in virus transmission[J]. J Virol, 2014, 88(18):10327-10339.
[14] Mocquet V, Neusiedler J, Rende F, et al. Nonsense-mediated mRNA decay inhibition by HTLV-1 Tax protein[J]. Retrovirology, 2014, 11(Suppl 1):O61.
[15] Wang W, Zhou J, Shi J, et al. Human T-cell leukemia virus type 1 Tax-deregulated autophagy pathway and c-FLIP expression contribute to resistance against death receptor-mediated apoptosis[J]. J Virol, 2014, 88(5):2786-2798.
[16] Parra E, Gutiérrez L. Growth inhibition of Tax-activated human Jurkat leukemia T cells by all-trans retinoic acid requires JNK-1 inhibition[J]. Oncol Rep, 2013, 29(1):387-393.
[17] Alais S, Dutartre H, Mahieux R. Quantitative analysis of human T-lymphotropic virus type 1(HTLV-1) infection using co-culture with Jurkat LTR-luciferase or Jurkat LTR-GFP reporter cells[J]. Methods Mol Biol, 2017, 1582:47-55.
[18] Kusano S, Yoshimitsu M, Hachiman M, et al. I-mfa domain proteins specifically interact with HTLV-1 Tax and repress its transactivating functions[J]. Virology, 2015, 486:219-227.
[19] Tanaka-Nakanishi A, Yasunaga J, Takai K, et al. HTLV-1 bZIP factor suppresses apoptosis by attenuating the function of FoxO3a and altering its localization[J]. Cancer Res, 2014, 74(1):188-200.
[20] Takiuchi Y, Kobayashi M, Tada K, et al. HTLV-1 bZIP factor suppresses TDP1 expression through inhibition of NRF-1 in adult T-cell leukemia[J]. Sci Rep, 2017, 7(1):12849.
[21] Nakamura H, Takahashi Y, Yamamoto-Fukuda T, et al. Direct infection of primary salivary gland epithelial cells by human T lymphotropic virus type I in patients with Sjögren's syndrome[J]. Arthritis Rheumatol, 2015, 67(4):1096-1106.
[22] Gross C, Wiesmann V, Millen S, et al. The Tax-inducible actin-bundling protein fascin is crucial for release and cell-to-cell transmission of human T-cell leukemia virus type 1(HTLV-1)[J]. PLoS Pathog, 2016, 12(10):e1005916.
[23] 杜伯雨, 白璐, 沈岩, 等. 肠道病毒EV71感染对T细胞免疫功能影响的研究[J]. 医学研究杂志, 2010, 39(8):50-53.
[24] Chen LC, Yeh TM. Enterovirus 71 infection of human immune cells induces the production of proinflammatory cytokines[J]. J Biomed Lab Sci, 2009, 21(3):82-89.
[25] 茌静, 何雅青, 余光清, 等. Toll样受体7在肠道病毒71型感染人Jurkat T细胞诱导炎症因子中的作用[J]. 中华预防医学杂志, 2016, 50(3):266-269.
[26] Siddiquey MN, Nakagawa H, Iwata S, et al. Anti-tumor effects of suberoylanilide hydroxamic acid on Epstein-Barr virus-associated T cell and natural killer cell lymphoma[J]. Cancer Sci, 2014, 105(6):713-722.
[27] Kawada J, Ito Y, Iwata S, et al. mTOR inhibitors induce cell-cycle arrest and inhibit tumor growth in Epstein-Barr virus-associated T and natural killer cell lymphoma cells[J]. Clin Cancer Res, 2014, 20(21):5412-5422.
[28] Huang WT, Lin CW. EBV-encoded miR-BART20-5p and miR-BART8 inhibit the IFN-γ-STAT1 pathway associated with disease progression in nasal NK-cell lymphoma[J]. Am J Pathol, 2014, 184(4):1185-1197.
[29] Chen S, Wang Z, Dai X, et al. Re-expression of microRNA-150 induces EBV-positive Burkitt lymphoma differentiation by modulating c-Myb in vitro[J]. Cancer Sci, 2013, 104(7):826-834.
[30] Teixeira JE, Heron BT, Huston CD. C1q-and collectin-dependent phagocytosis of apoptotic host cells by the intestinal protozoan Entamoeba histolytica[J]. J Infect Dis, 2008, 198(7):1062-1070.
[31] Lee YA, Kim KA, Min A, et al. Amoebic PI3K and PKC is required for Jurkat T cell death induced by Entamoeba histolytica[J]. Korean J Parasitol, 2014, 52(4):355-365.
[32] Domínguez-Villar M, Muñoz-Suano A, Anaya-Baz B, et al. Hepatitis C virus core protein up-regulates anergy-related genes and a new set of genes, which affects T cell homeostasis[J]. J Leukoc Biol, 2007, 82(5):1301-1310.
[33] Dominguez-Villar M, Fernandez-Ponce C, Munoz-Suano A, et al. Up-regulation of FOXP3 and induction of suppressive function in CD4⁺ Jurkat T-cells expressing hepatitis C virus core protein[J]. Clin Sci (Lond), 2012, 123(1):15-27.
[34] Park IW, Fan Y, Luo X, et al. HIV-1 Nef is transferred from expressing T cells to hepatocytic cells through conduits and enhances HCV replication[J]. PLoS One, 2014, 9(6):e99545.
[35] Parrula C, Fernandez SA, Landes K, et al. Success of measles virotherapy in ATL depends on type I interferon secretion and responsiveness[J]. Virus Res, 2014, 189:206-213.
[36] Achard C, Guillerme JB, Bruni D, et al. Oncolytic measles virus induces tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated cytotoxicity by human myeloid and plasmacytoid dendritic cells[J]. Oncoimmunology, 2016, 6(1):e1261240.
[37] Wolf K, Beimforde N, Falzarano D, et al. The Ebola virus soluble glycoprotein (sGP) does not affect lymphocyte apoptosis and adhesion to activated endothelium[J]. J Infect Dis, 2011, 204 Suppl 3:S947-S952.
[38] Shim SH, Kim DS, Cho W, et al. Coxsackievirus B3 regulates T-cell infiltration into the heart by lymphocyte function-associated antigen-1 activation via the cAMP/Rap1 axis[J]. J Gen Virol, 2014, 95(Pt 9):2010-2018.
[39] Melana SM, Pogo BG. Molecular characterization of Jurkat cells persistently infected with vaccinia virus mutant vp811[J]. Intervirology, 2005, 48(2-3):89-96.
[40] Kobayashi M, Ishida K, Matsuo J, et al. Chlamydophila pneumoniae attachment and infection in low proteoglycan expressing human lymphoid Jurkat cells[J]. Microb Pathog, 2011, 51(3):209-216.
[41] Hirai I, Ebara M, Nakanishi S, et al. Jurkat cell proliferation is suppressed by Chlamydia (Chlamydophila) pneumoniae infection accompanied with attenuation of phosphorylation at Thr389 of host cellular p70S6K[J]. Immunobiology, 2013, 218(4):527-532.
[42] Ishida K, Kubo T, Saeki A, et al. Chlamydophila pneumoniae in human immortal Jurkat cells and primary lymphocytes uncontrolled by interferon-γ[J]. Microbes infect, 2013, 15(3):192-200.
[43] Azenabor AA, Cintrón-Cuevas J, Schmitt H, et al. Chlamydia trachomatis induces anti-inflammatory effect in human macrophages by attenuation of immune mediators in Jurkat T-cells[J]. Immunobiology, 2011, 216(12):1248-1255.
[44] Kubo T, Ishida K, Matsuo J, et al. Chlamydia trachomatis serovar L2 infection model using human lymphoid Jurkat cells[J]. Microb Pathog, 2012, 53(1):1-11.