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Transcriptomes of splenocytes from 16-week-old lupus-prone female NZB/NZW F1 mice and non-lupus-prone male NZB/NZW F1 and female BALB/c mice

ABSTRACT: Transcriptomic analysis of gene expression of splenocytes from 16-week-old female NZB/NZW F1 (BWF1) mice, which are prone to lupus, and comparison to gene expression of splenocytes from male BWF1 and female BALB/c mice, which are not prone to lupus. Results provide insight into the differences in immunological activities that make female BWF1 mice more susceptible to lupus.

ORGANISM(S): Mus musculus

PROVIDER: GSE167273 | GEO | 2021/04/01

REPOSITORIES: GEO

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Transcriptomes of splenocytes from 16-week-old lupus-prone female NZB/NZW F1 mice and non-lupus-prone male NZB/NZW F1 and female BALB/c mice

Project description:Transcriptomes of splenocytes from 16-week-old lupus-prone female NZB/NZW F1 mice and non-lupus-prone male NZB/NZW F1 and female BALB/c mice

| PRJNA704036 | ENA

Transcription profiling by array of spleen samples from male and female BWF1 lupus-prone mice to investigate sex hormone regulated genes

Project description:Goal of experiment: Identification of differentially expressed immune genes from male and female BWF1 lupus-prone mice. (Female incidence is higher than male--attempting to find sex hormone regulated genes that may contribute to this difference).

2007-12-04 | E-GEOD-2336 | biostudies-arrayexpress

Reversible SAHH inhibitor protects against glomerulonephritis in lupus-prone NZB/NZW F1 mice by modulating α-actinin-4 associated skeleton organization of podocytes

Project description:Glomerulonephritis is one of the major complications and causes of death in systemic lupus erythematosus (SLE). Podocytes can be injured in many forms of glomerular disease, characteristic changes are actin cytoskeleton reorganization of involved foot process. ACTN4, encodes α-actinin-4, an actin-binding and crosslinking protein localized to podocytes in renal glomerulus. Abnormal expression of α-actinin-4 in mice leads to proteinuria and podocyte damage. DZ2002, a reversible S-adenosyl-L-homocysteine hydrolase (SAHH) inhibitor with immunosuppressive properties and potent therapeutic activity against various autoimmune diseases in mice. Here, we found that DZ2002 could significantly ameliorate nephritis of lupus-prone mice. Our results showed that DZ2002 decreased the accumulation of α-actinin-4, inhibited expression of integrin-linked kinase and downstream phosphorylation of β1-integrin.

2019-11-12 | PXD010059 | Pride

Kidney gene expression profiles from a lupus nephritis mouse model: NZB X NZW F1 (BWF1) mice treated with IFN-alpha with adenovirus delivery.

Project description:We characterized the longitudinal gene expression profiles of kidneys from a lupus model nephtiris: NZB X NZW F1 (BWF1) mice treated with IFN-alpha using adenovirus delivery. Genes from biological processes such as IFN response, complement, Fc gamma receptors, immune recruitment, innate immune pattern recognition, antibody response and fibrosis,were upregulated in diseased kidneys.

2016-09-06 | GSE86423 | GEO

Effect of Sirolimus treatment on lupus nephritis in NZB/W F1 female mice

Project description:NZB/WF1 female mice spontaneously develop autoimmune lupus nephritis. Expression profiling of kidney tissue from (a) 12 week NZB/W F1 female mice defined as asymptomatic for lupus nephritis, (b) 36 and 42 week NZB/W F1 female mice defined as diseased/symptomatic for lupus nephritis and (c) 36 and 42 week NZB/W F1 female mice that are diseased/symptomatic for lupus nephritis and treated with Sirolimus was carried out. The goal of the study was to identify genes associated with lupus nephritis and modulated by Sirolimus, an inhibitor of mTOR. In addition, lupus nephritis genes resistant to Sirolimus therapy were also identfied This series of samples comprises of kidney tissue from (a) 12 week old NZB/W F1 female mice defined as asymptomatic for lupus nephritis (N=4), (b) 36 (N=3) and 42 week (N=3) old NZB/W F1 female mice defined as diseased/symptomatic for lupus nephritis and (c) 36 (N=3)and 42 (N=3) week old NZB/W F1 female mice that are asymptomatic for lupus nephritis on treatment with Sirolimus

2008-11-20 | E-GEOD-12024 | biostudies-arrayexpress

Effect of Sirolimus treatment on lupus nephritis in NZB/W F1 female mice

2008-11-21 | GSE12024 | GEO

SM934 treated lupus-prone NZB × NZW F1 mice by enhancing macrophage interleukin-10 production and suppressing pathogenic T cell development.

Project description:BackgroundArtemisinin and its derivatives were reported to possess strong regulatory effects on inflammation and autoimmune diseases. This study was designed to examine the therapeutic effects and underlying mechanisms of SM934, a water-soluble artemisinin analogue, on lupus-prone female NZB × NZW F(1) mice.Methodology/principal findingsNZB/W F(1) mice were treated orally with SM934 for 3 or 6 months respectively to investigate the effect on clinical manifestations and immunological correlates. To further explore the mechanisms of SM934, ovalbumin (OVA)-immunized or interferon (IFN)-?-elicited C57BL/6 mice were used. In vivo, treatment with SM934 for 3 or 6 months significantly delayed the progression of glomerulonephritis and increased the survival rate of NZB/W F(1) mice. Clinical improvement was accompanied with decreased Th1-related anti-double-strand DNA (dsDNA) IgG2a and IgG3 Abs, serum interleukin (IL)-17, and increased Th2-related anti-dsDNA IgG1 Ab, serum IL-10 and IL-4. SM934 treatment also suppressed the accumulation of effector/memory T cells, induced the apoptosis of CD4(+) T cells, while enhancing the development of regulatory T cells in NZB/W F(1) mice. In addition, SM934 treatment promoted the IL-10 production of macrophages from NZB/W F(1) mice, OVA-immunized C57BL/6 mice and IFN-?-elicited C57BL/6 mice. In vitro, SM934 enhanced IL-10 production from primary macrophages stimulated with IFN-?.Conclusions/significanceThe results of this study demonstrated that artemisinin analogue SM934 had therapeutic effects on lupus-prone female NZB/W F(1) mice by inhibiting the pathogenic helper T cell development and enhancing anti-inflammatory cytokine IL-10 production.

| S-EPMC3289663 | biostudies-literature

Thymic B cells promote germinal center-like structures and the expansion of follicular helper T cells in lupus-prone mice

Project description:Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by autoantibody production and immune complex deposition. Previous evidence showed abnormal accumulation of B cells in the thymus of lupus-prone mice, but the role of this population remains undefined. We analyzed the distribution, function, and properties of thymic B cells in the BWF1 murine model of SLE. We found that B cells proliferate and cluster in germinal center-like structures along with autoantibody-secreting cells in the thymus of diseased-BWF1 mice. These thymic B cells induced the differentiation of follicular helper T cells (TFH). Our data suggest that the accumulation of B cells in the thymus of BWF1 mice results in the formation of germinal center-like structures and the expansion of TFH cells, which may favor the differentiation of autoreactive plasma cells. Therefore, the thymus emerges as a niche supporting the maintenance of the pathogenic humoral response in the development of murine SLE.

2020-03-24 | GSE147359 | GEO

Therapeutic effects of DZ2002, a reversible SAHH inhibitor, on lupus-prone NZB×NZW F1 mice via interference with TLR-mediated APC response.

Project description:AimTo examine the therapeutic effects and underlying mechanisms of DZ2002, a reversible S-adenosyl-L-homocysteine hydrolase (SAHH) inhibitor, on lupus-prone female NZB×NZW F1 (NZB/W F1) mice.MethodsFemale NZB/W F1 mice were treated orally with DZ2002 (0.5 mg·kg(-1)·d(-1)) for 11 weeks, and the proteinuria level and body weight were monitored. After the mice ware euthanized, serum biochemical parameters and renal damage were determined. Splenocytes of NZB/W F1 mice were isolated for ex vivo study. Toll-like receptor (TLR)-stimulated human peripheral blood mononuclear cells (PBMCs) or murine bone marrow-derived dendritic cells (BMDCs) were used for in vitro study.ResultsTreatment of the mice with DZ2002 significantly attenuated the progression of glomerulonephritis and improved the overall health. The improvement was accompanied by decreased levels of nephritogenic anti-dsDNA IgG2a and IgG3 antibodies, serum IL-17, IL-23p19 and TGF-?. In ex vivo studies, treatment of the mice with DZ2002 suppressed the development of pathogenic Th17 cells, significantly decreased IL-17, TGF-?, IL-6, and IL-23p19 production and impeded activation of the STAT3 protein and JNK/NF-?B signaling in splenocytes. DZ2002 (500 ?mol/L) significantly suppressed TLR agonists-stimulated up-regulation in IL-6, IL-12p40, TNF-?, and IgG and IgM secretion as well as in HLA-DR and CD40 expression of dendritic cells among human PBMCs in vitro. DZ2002 (100 ?mol/L) also significantly suppressed TLR agonists-stimulated up-regulation in IL-6 and IL-23p19 production in murine BMDCs, and prevented Th17 differentiation and suppressed IL-17 secretion by the T cells in a BMDC-T cell co-culture system.ConclusionDZ2002 effectively ameliorates lupus syndrome in NZB/W F1 mice by regulating TLR signaling-mediated antigen presenting cell (APC) responses.

| S-EPMC4651227 | biostudies-literature

Estrogen receptor alpha promotes lupus in (NZB×NZW)F1 mice in a B cell intrinsic manner.

Project description:Lupus is a systemic autoimmune disease characterized by the production of autoreactive antibodies against nuclear antigens. Women are disproportionately affected by lupus, and this sex bias is thought to be due, in large part, to the ability of estrogens to promote lupus pathogenesis. Previously, we have shown that global deletion of estrogen receptor alpha (ER?) significantly attenuated loss of tolerance, immune cell activation, autoantibody production, and the development of lupus nephritis. Here we show that targeted deletion of ER? specifically in B cells retards production of pathogenic autoantibodies and the development of nephritis in lupus-prone (NZB×NZW)F1 mice. Furthermore, we observed that ER? deletion in B cells was associated with decreased B cell activation in young, pre-autoimmune (NZB×NZW)F1 females. Altogether, these data suggest that ER? acts in a B cell-intrinsic manner to control B cell activation, autoantibody production, and lupus nephritis.

| S-EPMC5316311 | biostudies-literature

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