Dendritic cells exposed to estrogen in vitro exhibit therapeutic effects in ongoing experimental allergic encephalomyelitis

Pettersson, Åsa; Ciumas, Carolina; Chirsky, V. S.; Link, Hans; Huang, Yu‐Min; Xiao, Bao‐Guo

doi:10.1016/j.jneuroim.2004.07.004

Cited by 51 publications

(36 citation statements)

References 37 publications

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“…Recent evidence indicates that the induction of tolerogenic DCs by these factors could participate in such an immunosuppressive effect. Thus, corticosteroids [20], estrogens [21], and other hormone-like substances, such as vitamin D3 analogs [22], were found to induce DCs with tolerogenic capacity (also reviewed in this issue of Human Immunology). In this review, we will focus on the effects on immune tolerance of some anti-inflammatory neuropeptides.…”

Section: Tuning the Immune System With Neuroendocrine Mediatorsmentioning

confidence: 99%

Generating tolerogenic dendritic cells with neuropeptides

Delgado¹

2009

Human Immunology

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Section: Tuning the Immune System With Neuroendocrine Mediatorsmentioning

confidence: 99%

Generating tolerogenic dendritic cells with neuropeptides

Delgado¹

2009

Human Immunology

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“…In this study, we demonstrate that NGF can promote LPS-induced maturation of DCs both phenotypically and functionally by up-regulating expression of MHC class II and costimulatory molecules CD40, CD83, CD80, and CD86, production of Th1 cytokine IL-12, and proinflammatory cytokines IL-1␤, IL-6 and TNF-␣. As we know, DCs are involved in the pathogenesis of some kinds of neurological autoimmune and inflammatory diseases (37). Together with other reports such as the constitutive expression of neurotrophins receptor by Th1 but not Th0/Th2 clones (38), our study may provide another new mechanism for the involvement of NGF in the pathogenesis of neurological autoimmune and inflammatory diseases through promotion of DCs maturation, thus resulting in more production of proinflammatory cytokines, and activation of T cells causing damages to neurological cells or tissues.…”

Section: Activation Of P38mapk and Nf-b Pathways Is Required For The mentioning

confidence: 99%

Nerve Growth Factor Promotes TLR4 Signaling-Induced Maturation of Human Dendritic Cells In Vitro through Inducible p75NTR 1

Jiang

Chen

Zhang

et al. 2007

The Journal of Immunology

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Nerve growth factor (NGF) has been shown to play important roles in the differentiation, function, and survival of immune cells, contributing to immune responses and pathogenesis of autoimmune diseases. Dendritic cells (DCs) are a potent initiator for immune and inflammatory responses upon recognition of pathogens via Toll-like receptors (TLR). However, expression of NGF and its receptors on human monocyte-derived DCs (MoDCs) and the role of NGF in the response of DCs to TLR ligands remain to be investigated. In the present study, we demonstrate that there were weak expressions of NGF and no expression of NGF receptors p140TrkA and p75NTR on human immature MoDCs, however, the expression of NGF and p75NTR on MoDCs could be significantly up-regulated by LPS in a dose- and time-dependent manner. NGF could markedly promote LPS-induced expression of HLA-DR, CD40, CD80, CD83, CD86, CCR7, secretion of IL-12p40 and proinflammatory cytokines IL-1, IL-6, TNF-α, and the T cell-stimulating capacity of MoDCs, indicating that NGF can promote LPS-induced DC maturation. The promoting effect of NGF on LPS-induced MoDCs maturation could be completely abolished by pretreatment of MoDCs with p75NTR antagonist, suggesting that LPS-induced p75NTR mediates the effect. Furthermore, increased activation of the p38MAPK and NF-κB pathways has been shown to be responsible for the NGF-promoted DC maturation. Therefore, NGF facilitates TLR4 signaling-induced maturation of human DCs through LPS-up-regulated p75NTR via activation of p38 MAPK and NF-κB pathways, providing another mechanism for the involvement of NGF in the immune responses and pathogenesis of autoimmune diseases.

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“…[12][13][14] Several groups have shown that estrogen administration leads to clinical improvement in experimental autoimmune encephalomyelitis due to changes in DC function and the promotion of a Th2 immune response. 15 In contrast, disease exacerbation in systemic lupus erythematosus (SLE) patients has also been reported during pregnancy. 16 With regard to immunity to virus infection, Jilani et al reported that higher levels of sex steroid hormones during pregnancy correlate with the onset of fulminant viral hepatitis.…”

Section: Introductionmentioning

confidence: 99%

Estrogen inhibits dendritic cell maturation to RNA viruses

Escribese

Kraus

Rhee³

et al. 2008

Blood

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Dendritic cells (DCs) play a central role in initiating and polarizing the immune response. Therefore, DC maturation represents a key control point in the shift from innate to adaptive immunity. It is suspected that during pregnancy, hormones are critical factors that modulate changes reported to occur in maternal immunity. Here we examined the effect of 17-beta-estradiol (E2) on the maturational response triggered by virus in human DCs and its influence on their ability to activate naive T cells. We developed an in vitro system to measure the response of DCs to virus infection with Newcastle disease virus (NDV) after a 24-hour E2 treatment. Using this system, we demonstrated that E2 pretreatment down-regulated the antiviral response to RNA viruses in DCs by profoundly suppressing type I interferon (IFN) synthesis and other important inflammatory products. In addition, the DCs capacity to stimulate naive CD4 T cells was also reduced. These results suggest an important role for E2 in suppressing the antiviral response and provide a mechanism for the reduced immunity to virus infection observed during pregnancy.

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Dendritic cells exposed to estrogen in vitro exhibit therapeutic effects in ongoing experimental allergic encephalomyelitis

Cited by 51 publications

References 37 publications

Generating tolerogenic dendritic cells with neuropeptides

Generating tolerogenic dendritic cells with neuropeptides

Nerve Growth Factor Promotes TLR4 Signaling-Induced Maturation of Human Dendritic Cells In Vitro through Inducible p75NTR 1

Estrogen inhibits dendritic cell maturation to RNA viruses

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