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Topical TWEAK Accelerates Healing of Experimental Burn Wounds in Mice SCIE PubMed Scopus
期刊论文 | 2018 , 9 | FRONTIERS IN PHARMACOLOGY
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Abstract :

The interaction of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor inducible 14 (Fn14) participates in inflammatory responses, fibrosis, and tissue remodeling, which are central in the repair processes of wounds. Fn14 is expressed in main skin cells including dermal fibroblasts. This study was designed to explore the therapeutic effect of TWEAK on experimental burn wounds and the relevant mechanism underlying such function. Third-degree burns were introduced in two BALB/c mouse strains. Recombinant TWEAK was administrated topically, followed by the evaluation of wound areas and histologic changes. Accordingly, the downstream cytokines, inflammatory cell infiltration, and extracellular matrix synthesis were examined in lesional tissue. Moreover, the differentiation markers were analyzed in cultured human dermal fibroblasts upon TWEAK stimulation. The results showed that topical TWEAK accelerated the healing of burn wounds in wild-type mice but not in Fn14-deficient mice. TWEAK strengthened inflammatory cell infiltration, and exaggerated the production of growth factor and extracellular matrix components in wound areas of wild-type mice. Moreover, TWEAK/Fn14 activation elevated the expression of myofibroblastic differentiation markers, including alpha-smooth muscle actin and palladin, in cultured dermal fibroblasts. Therefore, topical TWEAK exhibits therapeutic effect on experimental burn wounds through favoring regional inflammation, cytokine production, and extracellular matrix synthesis. TWEAK/Fn14 activation induces the myofibroblastic differentiation of dermal fibroblasts, partially contributing to the healing of burn wounds.

Keyword :

animal model TWEAK burn wound differentiation dermal fibroblast Fn14

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GB/T 7714 Liu, Jing , Pang, Lingling , Liu, Yale et al. Topical TWEAK Accelerates Healing of Experimental Burn Wounds in Mice [J]. | FRONTIERS IN PHARMACOLOGY , 2018 , 9 .
MLA Liu, Jing et al. "Topical TWEAK Accelerates Healing of Experimental Burn Wounds in Mice" . | FRONTIERS IN PHARMACOLOGY 9 (2018) .
APA Liu, Jing , Pang, Lingling , Liu, Yale , Wu, Kunyi , Wang, Sijia , Wang, Xuening et al. Topical TWEAK Accelerates Healing of Experimental Burn Wounds in Mice . | FRONTIERS IN PHARMACOLOGY , 2018 , 9 .
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Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice SCIE PubMed
期刊论文 | 2018 | JOURNAL OF IMMUNOLOGY RESEARCH
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Many studies have demonstrated that anti-dsDNA IgG is closely associated with lupus nephritis. Recently, it was found that activation of the fibroblast growth factor-inducible 14 (Fn14) signaling pathway damages glomerular filtration barrier in MRL/lpr lupus-prone mice. However, MRL/lpr mice have high titers of serum autoantibodies other than anti-dsDNA IgG. The aim of this study was to further explore the effect of Fn14 deficiency on anti-dsDNA IgG-induced glomerular damage in severe combined immunodeficiency (SCID) mice that have no endogenous IgG. Fn14 deficiency was generated in SCID mice. The murine hybridoma cells producing control IgG or anti-dsDNA IgG were intraperitoneally injected into mice. In two weeks, the urine, serum, and kidney tissue samples were harvested from mice at sacrifice. It showed that the injection of anti-dsDNA IgG, but not control IgG hybridoma cells, induced proteinuria and glomerular damage in SCID mice. Between the wild-type (WT) and knockout (KO) mice injected with anti-dsDNA IgG hybridoma cells, the latter showed a decrease in both proteinuria and glomerular IgG deposition. The histopathological changes, inflammatory cell infiltration, and proinflammatory cytokine production were also attenuated in the kidneys of the Fn14-KO mice upon anti-dsDNA IgG injection. Therefore, Fn14 deficiency effectively protects SCID mice from anti-dsDNA IgG-induced glomerular damage.

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GB/T 7714 Wu, Jiawen , Min, Xiaoyun , Wang, Li et al. Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice [J]. | JOURNAL OF IMMUNOLOGY RESEARCH , 2018 .
MLA Wu, Jiawen et al. "Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice" . | JOURNAL OF IMMUNOLOGY RESEARCH (2018) .
APA Wu, Jiawen , Min, Xiaoyun , Wang, Li , Yang, Jie , Wang, Ping , Liu, Xingyin et al. Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice . | JOURNAL OF IMMUNOLOGY RESEARCH , 2018 .
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Tumor Necrosis Factor Receptor Mediates Fibroblast Growth Factor-Inducible 14 Signaling SCIE Scopus
期刊论文 | 2017 , 43 (2) , 579-588 | CELLULAR PHYSIOLOGY AND BIOCHEMISTRY | IF: 5.5
WoS CC Cited Count: 3 SCOPUS Cited Count: 4
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Abstract :

Tumor necrosis factor (TNF)-related weak inducer of apoptosis (TWEAK) engages its sole receptor, fibroblast growth factor-inducible 14 (Fn14), which participates in various inflammatory and immunologic processes. TWEAK/Fn14 interaction induces different cell fates depending on the local microenvironment, which correlates with certain expression profiles of TNF receptors (TNFR). The predominant expression of TNFR1 or TNFR2 facilitates cell death or proliferation, respectively, on TWEAK/Fn14 activation. TNFR-associated factors (TRAF) interact with Fn14, cellular inhibitor of apoptosis protein (cIAP)-1, and TNFR, consequently transducing signals from TWEAK to downstream cytokines and cell cycle mediators. An Fn14-TRAF2-TNFR axis has been suggested in the function of TWEAK/Fn14 signaling, which may serve as a target in the development of novel therapeutic strategies for many diseases that have Fn14-overexpressing cells in affected tissues. The aims of this review are: 1) to present the main results on TWEAK/Fn14 regulation of cell fates, 2) to analyze the mechanism of the Fn14-TRAF2-TNFR axis, and 3) to summarize the potential strategies in the pharmacologic targeting of this axis. (C) 2017 The Author(s) Published by S. Karger AG, Basel

Keyword :

Keratinocyte Proliferation TNFR TWEAK TRAF Apoptosis Fn14

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GB/T 7714 Wang, Xuening , Xiao, Shengxiang , Xia, Yumin . Tumor Necrosis Factor Receptor Mediates Fibroblast Growth Factor-Inducible 14 Signaling [J]. | CELLULAR PHYSIOLOGY AND BIOCHEMISTRY , 2017 , 43 (2) : 579-588 .
MLA Wang, Xuening et al. "Tumor Necrosis Factor Receptor Mediates Fibroblast Growth Factor-Inducible 14 Signaling" . | CELLULAR PHYSIOLOGY AND BIOCHEMISTRY 43 . 2 (2017) : 579-588 .
APA Wang, Xuening , Xiao, Shengxiang , Xia, Yumin . Tumor Necrosis Factor Receptor Mediates Fibroblast Growth Factor-Inducible 14 Signaling . | CELLULAR PHYSIOLOGY AND BIOCHEMISTRY , 2017 , 43 (2) , 579-588 .
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TWEAK/Fn14 Activation Participates in Skin Inflammation SCIE PubMed Scopus
期刊论文 | 2017 | MEDIATORS OF INFLAMMATION | IF: 3.549
WoS CC Cited Count: 4 SCOPUS Cited Count: 6
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Abstract :

Tumor necrosis factor-(TNF-) like weak inducer of apoptosis (TWEAK) participates in multiple biological activities via binding to its sole receptor-fibroblast growth factor-inducible 14 (Fn14). The TWEAK/Fn14 signaling pathway is activated in skin inflammation and modulates the inflammatory responses of keratinocytes by activating nuclear factor-kappa B signals and enhancing the production of several cytokines, including interleukins, monocyte chemotactic protein-1, RANTES (regulated on activation, normal T cell expressed and secreted), and interferon gamma-induced protein 10. Mild or transient TWEAK/Fn14 activation contributes to tissular repair and regeneration while excessive or persistent TWEAK/Fn14 signals may lead to severe inflammatory infiltration and tissue damage. TWEAK also regulates cell fate of keratinocytes, involving the function of Fn14-TNF receptor-associated factor-TNF receptor axis. By recruiting inflammatory cells, promoting cytokine production, and regulating cell fate, TWEAK/Fn14 activation plays a pivotal role in the pathogenesis of various skin disorders, such as psoriasis, atopic dermatitis, cutaneous vasculitis, human papillomavirus infection and related skin tumors, and cutaneous autoimmune diseases. Therefore, the TWEAK/Fn14 pathway may be a potential target for the development of novel therapeutics for skin inflammatory diseases.

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GB/T 7714 Liu, Qilu , Xiao, Shengxiang , Xia, Yumin . TWEAK/Fn14 Activation Participates in Skin Inflammation [J]. | MEDIATORS OF INFLAMMATION , 2017 .
MLA Liu, Qilu et al. "TWEAK/Fn14 Activation Participates in Skin Inflammation" . | MEDIATORS OF INFLAMMATION (2017) .
APA Liu, Qilu , Xiao, Shengxiang , Xia, Yumin . TWEAK/Fn14 Activation Participates in Skin Inflammation . | MEDIATORS OF INFLAMMATION , 2017 .
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Roles of tumour necrosis factor-related weak inducer of apoptosis/fibroblast growth factor-inducible 14 pathway in lupus nephritis SCIE PubMed Scopus
期刊论文 | 2017 , 22 (2) , 101-106 | NEPHROLOGY | IF: 2.178
WoS CC Cited Count: 8
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Abstract :

As one of the manifestations of patients with systemic lupus erythematosus, lupus nephritis (LN) has high morbidity and mortality. Although the explicit mechanism of LN remains to be fully elucidated, there is increasing evidence to support the notion that tumour necrosis factor-related weak inducer of apoptosis (TWEAK), acting via its sole receptor, fibroblast growth factor-inducible 14 (Fn14), plays a pivotal role in such pathologic process. TWEAK/Fn14 interactions occur prominently in kidneys of LN, inducing inflammatory responses, angiogenesis, mesangial proliferation, filtration barrier injuries, renal fibrosis, etc. This review will specify the important roles of TWEAK/Fn14 pathway in the pathogenesis of LN with experimental data from cellular and animal models. Additionally, the raised levels of urinary and serum soluble TWEAK correlate with renal disease activity in patients with LN. The neutralizing antibodies targeting TWEAK or other approaches inhibiting TWEAK/Fn14 signals can attenuate renal damage in the murine lupus models. Therefore, to focus on TWEAK/Fn14 signalling may be promising in both clinical evaluation and the treatment of patients with LN. Summary at a Glance This review describes evidence supporting a pathogenic role for tumour necrosis factor-related weak inducer of apoptosis (TWEAK) in human and experimental lupus nephritis. Current understanding of TWEAK is integrated with known mechanisms of renal inflammation and fibrosis. This is highly relevant given early stage clinical studies with anti-TWEAK monoclonal antibodies.

Keyword :

fibroblast growth factor-inducible 14 glomerular basement membrane lupus nephritis proinflammatory cytokines tumour necrosis factor-related weak inducer of apoptosis

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GB/T 7714 Chen, Jingyun , Wei, Linlin , Xia, Yumin . Roles of tumour necrosis factor-related weak inducer of apoptosis/fibroblast growth factor-inducible 14 pathway in lupus nephritis [J]. | NEPHROLOGY , 2017 , 22 (2) : 101-106 .
MLA Chen, Jingyun et al. "Roles of tumour necrosis factor-related weak inducer of apoptosis/fibroblast growth factor-inducible 14 pathway in lupus nephritis" . | NEPHROLOGY 22 . 2 (2017) : 101-106 .
APA Chen, Jingyun , Wei, Linlin , Xia, Yumin . Roles of tumour necrosis factor-related weak inducer of apoptosis/fibroblast growth factor-inducible 14 pathway in lupus nephritis . | NEPHROLOGY , 2017 , 22 (2) , 101-106 .
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TWEAK/Fn14 Activation Contributes to the Pathogenesis of Bullous Pemphigoid SCIE PubMed Scopus
期刊论文 | 2017 , 137 (7) , 1512-1522 | JOURNAL OF INVESTIGATIVE DERMATOLOGY | IF: 6.448
WoS CC Cited Count: 10 SCOPUS Cited Count: 10
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Abstract :

TWEAK participates in various cellular effects by engaging its receptor of Fn14. Increased levels of soluble TWEAK are associated with systemic autoimmunity in patients with lupus erythematosus, rheumatoid arthritis, or dermatomyositis. However, the role of TWEAK in bullous pemphigoid (BP) remains unknown. In this study, we found an elevated serum level of TWEAK and a positive correlation between serum TWEAK and anti-BP180 antibodies. Immunohistochemistry showed strong TWEAK and Fn14 expression and implied an opposite relationship between the TWEAK and BP180 expression in skin samples from BP patients. In vitro TWEAK stimuli reduced BP180 expression in HaCaT cells and inhibited the adhesion of cells to the culture dish. Consistently, the transfection of Fn14 small interfering RNA preserved BP180 and protected cells from losing adherence. Moreover, such effect of TWEAK correlated with activation of the extracellular signal-regulated kinase and NF KB pathways and downstream ADAMs. By silencing ADAM17 with small interfering RNA, we showed that ADAM17 participated in TWEAK-induced BP180 loss. Therefore, TWEAK may contribute to the pathogenesis of BP by reducing BP180 expression and cellular adherence, involving the activation of ERK and NF-KB pathways. TWEAK may serve as a biomarker or therapeutic target of BP.

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GB/T 7714 Liu, Yale , Peng, Lingling , Li, Liang et al. TWEAK/Fn14 Activation Contributes to the Pathogenesis of Bullous Pemphigoid [J]. | JOURNAL OF INVESTIGATIVE DERMATOLOGY , 2017 , 137 (7) : 1512-1522 .
MLA Liu, Yale et al. "TWEAK/Fn14 Activation Contributes to the Pathogenesis of Bullous Pemphigoid" . | JOURNAL OF INVESTIGATIVE DERMATOLOGY 137 . 7 (2017) : 1512-1522 .
APA Liu, Yale , Peng, Lingling , Li, Liang , Liu, Chengfei , Hu, Xiao , Xiao, Shengxiang et al. TWEAK/Fn14 Activation Contributes to the Pathogenesis of Bullous Pemphigoid . | JOURNAL OF INVESTIGATIVE DERMATOLOGY , 2017 , 137 (7) , 1512-1522 .
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The acitretin and methotrexate combination therapy for psoriasis vulgaris achieves higher effectiveness and less liver fibrosis SCIE PubMed Scopus
期刊论文 | 2017 , 121 , 158-168 | PHARMACOLOGICAL RESEARCH | IF: 4.897
WoS CC Cited Count: 3 SCOPUS Cited Count: 2
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Abstract :

Both acitretin and methotrexate are effective in ameliorating psoriatic lesion. However, their combination has been seldom reported in the treatment of psoriasis because of the warning regarding the potential hepatotoxicity of the drug interactions. This study was designed to investigate the effectiveness of such combination therapy for psoriasis vulgaris, and the potential benefit as well as side effect during the treatment. Thirty-nine patients with psoriasis vulgaris were treated with acitretin, methotrexate or their combination or as control. Similarly, K14-VEGF transgenic psoriasis-like mice were treated with these drugs. Human primary keratinocytes and hepatic stellate cells were used for analyzing their effect in vitro. The results showed that the combination therapy exhibited higher effectiveness in remitting skin lesion, but did not significantly affect the liver function of both patients and mice. Moreover, the combination groups showed less elevation of profibrotic factors in sera when compared with methotrexate alone groups accordingly. Furthermore, primary keratinocytes expressed more involucrin as well as loricrin and proliferated more slowly on the combined stimulation. Interestingly, such combination treatment induced lower expression of profibrotic factors in hepatic stellate cells. In conclusion, the acitretin-methotrexate combination therapy for psoriasis vulgaris can achieve higher effectiveness and result in less liver fibrosis. (C) 2017 Elsevier Ltd. All rights reserved.

Keyword :

Psoriasis Keratinocyte Combination therapy Liver fibrosis Acitretin Methotrexate

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GB/T 7714 An, Jingang , Zhang, Dingwei , Wu, Jiawen et al. The acitretin and methotrexate combination therapy for psoriasis vulgaris achieves higher effectiveness and less liver fibrosis [J]. | PHARMACOLOGICAL RESEARCH , 2017 , 121 : 158-168 .
MLA An, Jingang et al. "The acitretin and methotrexate combination therapy for psoriasis vulgaris achieves higher effectiveness and less liver fibrosis" . | PHARMACOLOGICAL RESEARCH 121 (2017) : 158-168 .
APA An, Jingang , Zhang, Dingwei , Wu, Jiawen , Li, Jiong , Teng, Xiu , Gao, Xiaomin et al. The acitretin and methotrexate combination therapy for psoriasis vulgaris achieves higher effectiveness and less liver fibrosis . | PHARMACOLOGICAL RESEARCH , 2017 , 121 , 158-168 .
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BP180 Is Critical in the Autoimmunity of Bullous Pemphigoid SCIE PubMed Scopus
期刊论文 | 2017 , 8 | FRONTIERS IN IMMUNOLOGY | IF: 5.511
WoS CC Cited Count: 6 SCOPUS Cited Count: 9
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Bullous pemphigoid (BP) is by far the most common autoimmune blistering dermatosis that mainly occurs in the elderly. The BP180 is a transmembrane glycoprotein, which is highly immunodominant in BP. The structure and location of BP180 indicate that it is a significant autoantigen and plays a key role in blister formation. Autoantibodies from BP patients react with BP180, which leads to its degradation and this has been regarded as the central event in BP pathogenesis. The consequent blister formation involves the activation of complement-dependent or - independent signals, as well as inflammatory pathways induced by BP180/anti-BP180 autoantibody interaction. As a multi-epitope molecule, BP180 can cause dermal-epidermal separation via combining each epitope with specific immunoglobulin, which also facilitates blister formation. In addition, some inflammatory factors can directly deplete BP180, thereby leading to fragility of the dermal-epidermal junction and blister formation. This review summarizes recent investigations on the role of BP180 in BP pathogenesis to determine the potential targets for the treatment of patients with BP.

Keyword :

cytokine dermal-epidermal junction bullous pemphigoid BP180 autoantibody

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GB/T 7714 Liu, Yale , Li, Liang , Xia, Yumin . BP180 Is Critical in the Autoimmunity of Bullous Pemphigoid [J]. | FRONTIERS IN IMMUNOLOGY , 2017 , 8 .
MLA Liu, Yale et al. "BP180 Is Critical in the Autoimmunity of Bullous Pemphigoid" . | FRONTIERS IN IMMUNOLOGY 8 (2017) .
APA Liu, Yale , Li, Liang , Xia, Yumin . BP180 Is Critical in the Autoimmunity of Bullous Pemphigoid . | FRONTIERS IN IMMUNOLOGY , 2017 , 8 .
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Anti-Double-Stranded DNA IgG Participates in Renal Fibrosis through Suppressing the Suppressor of Cytokine Signaling 1 Signals SCIE PubMed Scopus
期刊论文 | 2017 , 8 | FRONTIERS IN IMMUNOLOGY | IF: 5.511
WoS CC Cited Count: 4 SCOPUS Cited Count: 4
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Suppressor of cytokine signaling 1 (SOCS1) participates in renal fibrosis by downregulating Janus kinase 2 (JAK2)/signal transducer and activator of transcription 1 (STAT1)-mediated cytokine signaling. Recently, it was found that anti-double-stranded DNA (dsDNA) IgG induces the synthesis of profibrotic cytokines by renal cells. To explore the potential effect of anti-dsDNA IgG on SOCS1-mediated renal fibrosis, kidney tissues were collected from patients with lupus nephritis (LN) as well as MRL/lpr lupus-prone mice. The SOCS1 expression was evaluated in tissue samples. In addition, SCID mice were injected with anti-dsDNA IgG, followed by evaluation of SOCS1 levels. Renal resident cells were cultured in vitro, receiving the stimulation of anti-dsDNA IgG and then the measurement of SOCS1, JAK2, STAT1 alpha, and profibrotic cytokines. Moreover, the binding of anti-dsDNA IgG to SOCS1 kinase inhibitory region (KIR) peptide was analyzed by surface plasmon resonance. We found that SOCS1 expression was inhibited, but JAK2/STAT1 activation was prominent in the kidney tissues of patients with LN, MRL/lpr mice, or anti-dsDNA IgG-injected SCID mice. The cultured renal cells also showed SOCS1 downregulation, JAK2/STAT1 activation, and profibrotic cytokine promotion upon anti-dsDNA IgG stimulation. Surprisingly, anti-dsDNA IgG showed high affinity to KIR peptide and competed with JAK2 loop for KIR. Additionally, a DNA-mimicking peptide (ALW) blocked the binding of anti-dsDNA IgG to KIR, and even partially abrogated the activation of JAK2/STAT1 alpha signals and the expression of profibrotic cytokines in SCID mice. In conclusion, anti-dsDNA IgG downregulates SOCS1 expression, activates JAK2/STAT1 signals, and contributes to renal fibrosis; its peptide blockade may restore the SOCS1 inhibitory effect on the production of profibrotic cytokine, and finally ameliorate renal fibrosis in LN.

Keyword :

suppressor of cytokine signaling 1 peptide lupus nephritis signal transducer and activator of transcription 1 anti-double-stranded DNA IgG Janus kinase 2 renal fibrosis

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GB/T 7714 Wang, Ping , Yang, Jie , Tong, Fang et al. Anti-Double-Stranded DNA IgG Participates in Renal Fibrosis through Suppressing the Suppressor of Cytokine Signaling 1 Signals [J]. | FRONTIERS IN IMMUNOLOGY , 2017 , 8 .
MLA Wang, Ping et al. "Anti-Double-Stranded DNA IgG Participates in Renal Fibrosis through Suppressing the Suppressor of Cytokine Signaling 1 Signals" . | FRONTIERS IN IMMUNOLOGY 8 (2017) .
APA Wang, Ping , Yang, Jie , Tong, Fang , Duan, Zhaoyang , Liu, Xingyin , Xia, Linlin et al. Anti-Double-Stranded DNA IgG Participates in Renal Fibrosis through Suppressing the Suppressor of Cytokine Signaling 1 Signals . | FRONTIERS IN IMMUNOLOGY , 2017 , 8 .
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The deposition of anti-DNA IgG contributes to the development of cutaneous lupus erythematosus SCIE PubMed Scopus
期刊论文 | 2017 , 191 , 1-9 | IMMUNOLOGY LETTERS | IF: 2.436
WoS CC Cited Count: 1
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Anti-DNA IgG is a hallmark of systemic lupus erythematosus and induces internal injuries in patients. It is known that cutaneous lupus erythematosus (CLE) involves the deposition of autoantibodies in the dermoepidermal junction of the skin and that anti-DNA IgG binds specifically to keratinocytes. However, the definite role of anti DNA IgG in CLE remains unclear. The purpose of this study was to elucidate the effect of anti-DNA IgG on keratinocytes in CLE. Skin tissues were collected from patients with CLE and healthy controls. Also, murine anti DNA IgG was incubated with frozen sections of murine skin or PAM212 keratinocytes. The chemotaxis of J774.2 macrophages was evaluated in special chambers with keratinocytes under anti-DNA IgG stimulation. Enzyme linked immunosorbent assay, flow cytometry, Western blot, and surface plasmon resonance were used to quantitate the interaction between anti-DNA IgG and keratinocyte-related self-antigens. The results showed that anti-DNA IgG could be eluted from the lesional tissues of CLE patients, depending on the serum positivity. Murine anti-DNA IgG bound preferably to the dermoepidermal zones of normal skin and specifically to collagen III and the suppressor of cytokine signalling 1 (SOCS1) but not to Ro52. Moreover, the chemotaxis of macrophages was promoted by the incubation of anti-DNA IgG with keratinocytes. Interestingly, anti-DNA IgG exaggerated both the expression and the activation of fibroblast growth factor inducible 14 (Fn14) in keratinocytes and regulated SOCS1 signals in a time-dependent manner. In conclusion, anti-DNA IgG may contribute to the development of CLE through binding to keratinocyte-related antigens, exacerbating inflammatory infiltration, and modulating Fn14 and SOCS1 pathways.

Keyword :

Collagen III Anti-DNA antibody Cutaneous lupus erythematosus Keratinocyte Cross reaction

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GB/T 7714 Dong, Yingying , Zhang, Yi , Xia, Linlin et al. The deposition of anti-DNA IgG contributes to the development of cutaneous lupus erythematosus [J]. | IMMUNOLOGY LETTERS , 2017 , 191 : 1-9 .
MLA Dong, Yingying et al. "The deposition of anti-DNA IgG contributes to the development of cutaneous lupus erythematosus" . | IMMUNOLOGY LETTERS 191 (2017) : 1-9 .
APA Dong, Yingying , Zhang, Yi , Xia, Linlin , Wang, Ping , Chen, Jingyun , Xu, Meifeng et al. The deposition of anti-DNA IgG contributes to the development of cutaneous lupus erythematosus . | IMMUNOLOGY LETTERS , 2017 , 191 , 1-9 .
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