Expression of TLR-7, MyD88, NF-kB, and INF-α in B Lymphocytes of Mayan Women with Systemic Lupus Erythematosus in Mexico

Valencia-Pacheco, Guillermo; Noh, Irene B. Novelo; Cárdenas, Rubí M.-H. Velasco; Ramírez, Angélica V. Angulo; Villanueva, Ricardo F. López; Ortiz, Irma G Quintal; Salomón, Ligia Gabriela Alonso; Ruz, Norma Pavía; Cárdenas, Nubia A. Rivero

doi:10.3389/fimmu.2016.00022

Cited by 33 publications

(24 citation statements)

References 57 publications

(42 reference statements)

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“… 34 As a common adaptor, MyD88 could interact with interleukin-1receptor-associated kinase 1/4 (IRAK1/4) and TNF receptor-associated factor 6 (TRAF6) through its amino-terminal death domain and induce the activation of NF-κB, thus enhancing the expression of pro-inflammatory factors. 35 , 36 It has been reported that the expression of MyD88 was aberrantly expressed in the B lymphocytes of SLE patients, 37 implying that MyD88 might be involved in the development and process of SLE. As the critical role of MyD88 in inflammatory response, we further investigated whether MyD88 was regulated by miR-145 and was associated with the IL-6-induced increase of sensitivity to UVB irradiation in HaCaT cells.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: MicroRNA-145 attenuates IL-6-induced enhancements of sensitivity to UVB irradiation by suppressing MyD88 in HaCaT cells

Dong

Jiang

Chen

et al. 2018

Int J Immunopathol Pharmacol

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MicroRNAs (miRNAs/miRs) play vital roles in various immune diseases including systemic lupus erythematosus (SLE). The current study aimed to assess the role of miR-145 in interleukin-6 (IL-6)-treated HaCaT cells under ultraviolet B (UVB) irradiation and further explore the potential regulatory mechanism. HaCaT cells were pretreated with IL-6 and then exposed to UVB to assess the effect of IL-6 on sensitivity of HaCaT cells to UVB irradiation. The levels of miR-145 and MyD88 were altered by transfection and the transfected efficiency was verified by quantitative reverse transcription polymerase chain reaction (qRT-PCR)/western blot analysis. Cell viability, percentage of apoptotic cells and expression levels of apoptosis-related factors were measured by trypan blue assay, flow cytometry assay, and western blot analysis, respectively. In addition, the levels of c-Jun N-terminal kinases (JNK) and nuclear factor-κB (NF-κB) signaling pathway-related factors were assessed by western blot analysis. IL-6 treatments significantly aggravated the reduction of cell viability and promotion of cell apoptosis caused by UVB irradiation in HaCaT cells. Interestingly, miR-145 level was augmented by UVB exposure and miR-145 mimic alleviated IL-6-induced increase of sensitivity to UVB irradiation in HaCaT cells, as dramatically increased cell viability and reduced cell apoptosis. Opposite effects were observed in miR-145 inhibitor-transfected cells. Meanwhile, MyD88 was negatively regulated by miR-145 and MyD88 mediated the regulatory effect of miR-145 on IL-6- and UVB-treated cells. In addition, miR-145 mimic inhibited the JNK and NF-κB pathways by down-regulating MyD88. In conclusion, the present study demonstrated that miR-145 alleviated IL-6-induced increase of sensitivity to UVB irradiation by down-regulating MyD88 in HaCaT cells.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: MicroRNA-145 attenuates IL-6-induced enhancements of sensitivity to UVB irradiation by suppressing MyD88 in HaCaT cells

Dong

Jiang

Chen

et al. 2018

Int J Immunopathol Pharmacol

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“…Increased mRNA expression of MyD88, TRAF6, and IRAK4 has been demonstrated in PBMCs from SLE patients, which correlated with disease activity (41). Increased expression of MyD88 in B lymphocytes was also found in SLE patients but unlikely to be affected by disease activity (42). Increased expression of MyD88, TRIF, and IRAK has been found in monocytes from patients with T1DM (20, 43).…”

Section: Discussionmentioning

confidence: 99%

Increased Toll-Like Receptors Activity and TLR Ligands in Patients with Autoimmune Thyroid Diseases

Peng

Wang

et al. 2016

Front. Immunol.

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ObjectiveAutoimmune thyroid disease (AITD) is an organ-specific disorder due to the interplay between environmental and genetic factors. Toll-like receptors (TLRs) are pattern recognition receptors expressed abundantly on monocytes. There is a paucity of data on TLR expression in AITD. The aim of this study was to examine TLR expression, activation, ligands, and downstream signaling adaptors in peripheral blood mononuclear cells (PBMCs) extracted from untreated AITD patients and healthy controls.MethodWe isolated PBMC of 30 healthy controls, 36 patients with untreated Hashimoto’s thyroiditis, and 30 patients with newly onset Graves’ disease. TLR mRNA, protein expression, TLR ligands, and TLR adaptor molecules were measured using real-time PCR, Western blot, flow cytometry, and enzyme-linked immunosorbent assay (ELISA). PBMC was simulated with TLR agonists. The effects of TLR agonists on the viability of human PBMC were evaluated using the MTT assay. The supernatants of cell cultures were measured for the pro-inflammatory cytokines, interleukin (IL)-6, tumor necrosis factor alpha (TNF-α), and IL-10 by ELISA.ResultsTLR2, TLR3, TLR9, and TLR10 mRNA were significantly increased in AITD patients compared with controls. TLR2, TLR3, TLR9, high mobility group box 1 (HMGB1), and RAGE expression on monocytes was higher in patients than control at baseline and TLR agonists’ stimulation. The release of TNF-α and IL-6 was significantly increased in PBMCs from AITD patients with TLR agonists, while IL-10 was significantly decreased. Downstream targets of TLR, myeloid differentiation factor 88 (MyD88), and myeloid toll/IL-1 receptor-domain containing adaptor-inducing interferon-β were significantly elevated in AITD patients. Levels of TLR2 ligands, HMGB1, and heat shock protein 60 were significantly elevated in AITD patients compared with those in controls and positively correlated with TgAb and TPOAb, while sRAGE concentration was significantly decreased in AITD patients.ConclusionThis work is the first to show that TLR2, TLR3, and TLR9 expression and activation are elevated in the PBMCs of patients with AITD and TLRs may participate in the pathogenesis of AITD.

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“…20 Mayyan women are more suitable to get lupus disease. Pacheo et al 21 assess the role of TLR7, MyD88, and NF-κB p65 in B-lymphocytes of Mayan women with SLE and point out the increased expression of TLR7, MyD88, and NF-κB p65 in B-lymphocytes from Mayan women, which supports its role in the pathogenesis of SLE in this ethnic population of southeast of Mexico.…”

Section: 4mentioning

confidence: 92%

Involvement of NF-κB Signaling Pathway in the Pathogenesis of Systemic Lupus Erythematosus

Mishra¹

2016

Nephrol Open J

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Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by accumulation of anti-nuclear autoantibodies, hyperactivation. It can affect any organ, including brain, skin, joint, and kidney. The nuclear NF-κB pathway has long been considered a crucial pro-inflammatory signaling pathway. Its transcribed the genes involves in various autoimmune disease. Within the past year, many research studies have been conducted the role of NF-κB signaling in lupus. In this review, we will highlight some recent studies that support the potential link of NF-κB signaling pathway which play a crucial role in the pathogenesis of SLE.

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Expression of TLR-7, MyD88, NF-kB, and INF-α in B Lymphocytes of Mayan Women with Systemic Lupus Erythematosus in Mexico

Cited by 33 publications

References 57 publications

RETRACTED: MicroRNA-145 attenuates IL-6-induced enhancements of sensitivity to UVB irradiation by suppressing MyD88 in HaCaT cells

RETRACTED: MicroRNA-145 attenuates IL-6-induced enhancements of sensitivity to UVB irradiation by suppressing MyD88 in HaCaT cells

Increased Toll-Like Receptors Activity and TLR Ligands in Patients with Autoimmune Thyroid Diseases

Involvement of NF-κB Signaling Pathway in the Pathogenesis of Systemic Lupus Erythematosus

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