RETRACTED: TGF-β1 re-programs TLR4 signaling in L. donovani infection: enhancement of SHP-1 and ubiquitin-editing enzyme A20 (Retracted article. See vol. 101, pg. 91, 2023)

被引：30

作者：

Das, Sushmita ^{[1
,2
]}

Pandey, Krishna ^{[1
,2
]}

Kumar, Ashish ^{[1
,2
]}

Sardar, Abul H. ^{[1
,2
]}

Purkait, Bidyut ^{[1
,2
]}

Kumar, Manish ^{[1
,2
]}

Kumar, Sudeep ^{[3
]}

Ravidas, Vidya N. ^{[1
,2
]}

Roy, Syamal ^{[4
]}

Singh, Dharmendra ^{[1
,2
]}

Das, Pradeep ^{[1
,2
]}

机构：

[1] Indian Council Med Res, Rajendra Mem Res Inst Med Sci, Dept Mol Parasitol, Patna 800007, Bihar, India

[2] Indian Council Med Res, Rajendra Mem Res Inst Med Sci, Dept Clin Med, Patna 800007, Bihar, India

[3] Univ New Mexico, Sch Med, Dept Internal Med, Div Infect Dis,Inst Global Hlth, Albuquerque, NM 87131 USA

[4] Indian Inst Chem Biol CSIR, Dept Infect Dis, Kolkata, India

来源：

IMMUNOLOGY AND CELL BIOLOGY | 2012年 / 90卷 / 06期

关键词：

leishmaniasis; Toll-like receptors; TGF-beta(1); SHP-1; A20; PROTEIN-TYROSINE-PHOSPHATASE; NF-KAPPA-B; RECEPTOR-ASSOCIATED KINASE; ENDOTOXIN TOLERANCE; TNF-ALPHA; LEISHMANIA; MACROPHAGES; INHIBITION; ACTIVATION; GROWTH;

D O I：

10.1038/icb.2011.80

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Visceral leishmaniasis (VL), caused by Leishmania donovani, is a major health concern in India. It represents T-helper type 2 (Th2) bias of cytokines in active state and Th1 bias at cure. However, the role of the parasite in regulating Toll-like receptor (TLR)-mediated macrophage activation in VL patients remains elusive. In this report, we demonstrated that later stages of L. donovani infection rendered tolerance to macrophages, leading to incapability for the production of inflammatory cytokines like tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta in response to TLR stimulation. Overexpression of transforming growth factor (TGF)-beta(1), but not IL-10, resulted in suppressed lipopolysaccharide (LPS)-induced production of TNF-alpha and downregulation of TLR4 expression in L. donovani-infected macrophages. Recombinant human (rh)TGF-beta(1) markedly enhanced tyrosine phosphatase (Src homology region 2 domain-containing phosphatase-1) activity, but inhibited IL-1 receptor-activated kinase (IRAK)-1 activation. Addition of neutralizing TGF-beta(1) antibody reversed these effects, and thus suggesting the pivotal role of TGF-beta(1) in promoting refractoriness for LPS in macrophages. Surprisingly, the use of a tyrosine phosphatase inhibitor (sodium orthovanadate, Na3VO4) promoted IRAK-1 activation, confirming the negative inhibitory role of tyrosine phosphatase in macrophage activation. Furthermore, rhTGF-beta(1) induced tolerance in infected macrophages by reducing inhibitory protein (I kappa B alpha) degradation in a time-dependent manner. In addition, short interfering RNA studies proved that overexpression of A20 ubiquitin-editing protein complex induced inhibitory activity of TGF-beta(1) on LPS-mediated nuclear factor-kappa B activation. Thus, these findings suggest that TGF-beta(1) promotes overexpression of A20 through tyrosine phosphatase activity that ensures transient activation of inflammatory signaling pathways in macrophages in active L. donovani infection. Immunology and Cell Biology (2012) 90, 640-654; doi:10.1038/icb.2011.80; published online 4 October 2011

引用

页码：640 / 654

页数：15

共 55 条

[1] Leishmania-Induced IRAK-1 Inactivation Is Mediated by SHP-1 Interacting with an Evolutionarily Conserved KTIM Motif [J].

Abu-Dayyeh, Issa ;

Shio, Marina Tiemi ;

Sato, Shintaro ;

Akira, Shizuo ;

Cousineau, Benoit ;

Olivier, Martin .

PLOS NEGLECTED TROPICAL DISEASES, 2008, 2 (12)

[2] Toll-like receptors in the induction of the innate immune response [J].

Aderem, A ;

Ulevitch, RJ .

NATURE, 2000, 406 (6797) :782-787

[3] Gamma interferon and granulocyte/monocyte colony-stimulating factor prevent endotoxin tolerance in human monocytes by promoting interleukin-1 receptor-associated kinase expression and its association to MyD88 and not by modulating TLR4 expression [J].

Adib-Conquy, M ;

Cavaillon, JM .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (31) :27927-27934

[4] Phosphatase SHP-1 promotes TLR- and RIG-I-activated production of type I interferon by inhibiting the kinase IRAK1 [J].

An, Huazhang ;

Hou, Jin ;

Zhou, Jun ;

Zhao, Wei ;

Xu, Hongmei ;

Zheng, Yuejuan ;

Yu, Yizhi ;

Liu, Shuxun ;

Cao, Xuetao .

NATURE IMMUNOLOGY, 2008, 9 (05) :542-550

[5] TGF-β-regulated tyrosine phosphatases induce lymphocyte apoptosis in Leishmania donovani-infected hamsters [J].

Banerjee, Rajdeep ;

Kumar, Sudeep ;

Sen, Abhik ;

Mookerjee, Ananda ;

Roy, Syamal ;

Pal, Subrata ;

Das, Pradeep .

IMMUNOLOGY AND CELL BIOLOGY, 2011, 89 (03) :466-474

[6] TRANSFORMING GROWTH-FACTOR-BETA IN LEISHMANIAL INFECTION - A PARASITE ESCAPE MECHANISM [J].

BARRALNETTO, M ;

BARRAL, A ;

BROWNELL, CE ;

SKEIKY, YAW ;

ELLINGSWORTH, LR ;

TWARDZIK, DR ;

REED, SG .

SCIENCE, 1992, 257 (5069) :545-548

[7] Leishmania major parasites induced macrophage tolerance: Implication of MAPK and NF-κB pathways [J].

Ben-Othman, Rym ;

Dellagi, Koussay ;

Guizani-Tabbane, Lamia .

MOLECULAR IMMUNOLOGY, 2009, 46 (16) :3438-3444

[8] A novel approach to regulate experimental visceral leishmaniasis in murine macrophages using CCR5 siRNA [J].

Bhattacharyya Majumdar, S. ;

Dey, R. ;

Majumder, N. ;

Bhattacharjee, S. ;

Majumdar, S. .

SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 2008, 67 (04) :345-353

[9] The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses [J].

Boone, DL ;

Turer, EE ;

Lee, EG ;

Ahmad, RC ;

Wheeler, MT ;

Tsui, C ;

Hurley, P ;

Chien, M ;

Chai, S ;

Hitotsumatsu, O ;

McNally, E ;

Pickart, C ;

Ma, A .

NATURE IMMUNOLOGY, 2004, 5 (10) :1052-1060

[10] A20: Central Gatekeeper in Inflammation and Immunity [J].

Coornaert, Beatrice ;

Carpentier, Isabelle ;

Beyaert, Rudi .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2009, 284 (13) :8217-8221

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