Bystander suppression of murine collagen-induced arthritis by long-term nasal administration of a self type II collagen peptide

Bayrak, S; Mitchison, N. A.

doi:10.1046/j.1365-2249.1998.00638.x

Cited by 16 publications

(17 citation statements)

References 28 publications

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“…Therefore, chronic Ag-specific Th2 inflammation can potentiate further naive T cell sensitization to distinct allergens in a process we have called collateral priming (Table I). We have used the term collateral priming to describe the process of activation of naive T cells to their cognate Ag by adaptive immune signals to contrast it with the phenomena known as bystander activation (32)(33)(34)(35). Although both processes involve activation of T cells by factors produced by a proximal but distinct T cell population, collateral priming is the activation of a naive T cell to its cognate Ag (as compared with an Ag-nonspecific response).…”

Section: Discussionmentioning

confidence: 99%

IL-4-Dependent Th2 Collateral Priming to Inhaled Antigens Independent of Toll-Like Receptor 4 and Myeloid Differentiation Factor 88

Eisenbarth¹,

Zhadkevich²,

Ranney³

et al. 2004

The Journal of Immunology

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Allergic asthma is an inflammatory lung disease thought to be initiated and directed by type 2 helper T cells responding to environmental Ags. The mechanisms by which allergens induce Th2-adaptive immune responses are not well understood, although it is now clear that innate immune signals are required to promote DC activation and Th2 sensitization to inhaled proteins. However, the effect of ongoing Th2 inflammation, as seen in chronic asthma, on naive lymphocyte activation has not been explored. It has been noted that patients with atopic disorders demonstrate an increased risk of developing sensitivities to new allergens. This suggests that signals from an adaptive immune response may facilitate sensitization to new Ags. We used a Th2-adoptive transfer murine model of asthma to identify a novel mechanism, termed “collateral priming,” in which naive CD4+ T cells are activated by adaptive rather than innate immune signals. Th2 priming to newly encountered Ags was dependent on the production of IL-4 by the transferred Th2 population but was independent of Toll-like receptor 4 signaling and the myeloid differentiation factor 88 Toll-like receptor signaling pathway. These results identify a novel mechanism of T cell priming in which an Ag-specific adaptive immune response initiates distinct Ag-specific T cell responses in the absence of classical innate immune system triggering signals.

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Section: Discussionmentioning

confidence: 99%

IL-4-Dependent Th2 Collateral Priming to Inhaled Antigens Independent of Toll-Like Receptor 4 and Myeloid Differentiation Factor 88

Eisenbarth¹,

Zhadkevich²,

Ranney³

et al. 2004

The Journal of Immunology

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“…In this sense, eye-induced tolerance is a promising therapeutic tool in the treatment of complicated autoimmune diseases such as CIA [37,38] or EAE [39–41]. Several tolerance protocols are being proposed for controlling inflammatory manifestations, in particular autoimmune diseases such as colitis [42–48]. …”

Section: Resultsmentioning

confidence: 99%

“…The effects of bystander suppression is related to the secretion of cytokines such as TGF-β, IL-4 and IL-10, and by the action of regulatory T cells [42,91,92]. …”

Section: Resultsmentioning

confidence: 99%

“…Thus, the suppressive response initiated by mucosal administration of dietary proteins associated with self-antigens has been gaining ground as a preventive or therapeutic intervention proposed for autoimmune diseases [24,42,48]. In this respect, several authors have shown that the oral tolerance to dietary antigens may prevent or inhibit the progression of systemic or organ-specific autoimmune diseases [34,35,93].…”

Section: Resultsmentioning

confidence: 99%

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Oral Tolerance Induced by OVA Intake Ameliorates TNBS-Induced Colitis in Mice

et al. 2017

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IntroductionLiterature data have shown that the consumption of dietary proteins may cause modulatory effects on the host immune system, process denominated oral tolerance by bystander suppression. It has been shown that the bystander suppression induced by dietary proteins can improve inflammatory diseases such as experimental arthritis. Here, we evaluated the effects of oral tolerance induced by ingestion of ovalbumin (OVA) on TNBS-induced colitis in mice, an experimental model for human Crohn’s disease.Methods and ResultsColitis was induced in BALB/c mice by instilling a single dose of TNBS (100 mg/kg) in ethanol into the colon. Tolerized mice received OVA (4mg/mL) dissolved in the drinking water for seven consecutive days, prior to or concomitantly with the intrarectal instillation. Control groups received protein-free water and ethanol by intrarectal route. We observed that either the prior or concomitant induction of oral tolerance were able to reduce the severity of colitis as noted by recovery of body weight gain, improvement of clinical signs and reduction of histological abnormalities. The in vitro proliferation of spleen cells from tolerant colitic mice was lower than that of control mice, the same as the frequencies of CD4+ T cells secreting IL-17 and IFN-γ. The frequencies of regulatory T cells and T cells secreting IL-10 have increased significantly in mice orally treated with OVA. The levels of inflammatory cytokines (IL-17A, TNF-α, IL-6 and IFN-γ) were lower in supernatants of cells from tolerant colitic mice, whereas IL-10 levels were higher.ConclusionOur data show that the modulation of immune response induced by oral tolerance reduces the severity of experimental colitis. Such modulation may be partially attributed to the increase of Treg cells and reduction of pro-inflammatory cytokines in peripheral lymphoid organs of tolerant mice by bystander suppression.

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“…CII, like myelin basic protein, can elicit tissue-specific autoimmune disease [38-40]. Some collagen derived peptides (e.g., CII 256-270 , CII 707-721 , and CII 1237-1249 ) have been used induce immunotolerance and have been shown to hinder the progression of CIA [41,42]. The selection of CII peptides used in this the present study was based on previous studies showing that certain epitopes such as CII 256-270 can bind to I-A q MHC class II molecules [40,43].…”

Section: Discussionmentioning

confidence: 99%

Bifunctional Peptide Inhibitors Suppress Interleukin-6 Proliferation and Ameliorates Murine Collagen-Induced Arthritis

Kiptoo¹

2014

J Clin Cell Immunol

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The objective of this study is to evaluate the efficacy and potential mechanism of action of type-II collagen bifunctional peptide inhibitor (CII-BPI) molecules in suppressing rheumatoid arthritis in the collagen-induced arthritis (CIA) mouse model. CII-BPI molecules (CII-BPI-1, CII-BPI-2, and CII-BPI-3) were formed through conjugation between an antigenic peptide derived from type-II collagen and a cell adhesion peptide LABL (CD11a237-246) from the I-domain of LFA-1 via a linker molecule. The hypothesis is that the CII-BPI molecules simultaneously bind to MHC-II and ICAM-1 on the surface of APC and block maturation of the immunological synapse. As a result, the differentiation of naïve T cells is altered from inflammatory to regulatory and/or suppressor T cells. The efficacies of CII-BPI molecules were evaluated upon intravenous injections in CIA mice. Results showed that CII-BPI-1 and CIIBPI-2 suppressed the joint inflammations in CIA mice in a dose-dependent manner and were more potent than the respective antigenic peptides alone. CII-BPI-3 was not as efficacious as CII-BPI-1 and CII-BPI-2. Significantly less joint damage was observed in CII-BPI-2 and CII-2 treated mice than in the control. The production of IL-6 was significantly lower at the peak of disease in mice treated with CII-BPI-2 compared to those treated with CII-2 and control. In conclusion, this is the first proof-of-concept study showing that BPI molecules can be used to suppress RA and may be a potential therapeutic strategy for the treatment of rheumatoid arthritis.

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Bystander suppression of murine collagen-induced arthritis by long-term nasal administration of a self type II collagen peptide

Cited by 16 publications

References 28 publications

IL-4-Dependent Th2 Collateral Priming to Inhaled Antigens Independent of Toll-Like Receptor 4 and Myeloid Differentiation Factor 88

IL-4-Dependent Th2 Collateral Priming to Inhaled Antigens Independent of Toll-Like Receptor 4 and Myeloid Differentiation Factor 88

Oral Tolerance Induced by OVA Intake Ameliorates TNBS-Induced Colitis in Mice

Bifunctional Peptide Inhibitors Suppress Interleukin-6 Proliferation and Ameliorates Murine Collagen-Induced Arthritis

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