Suppression of collagen-induced arthritis with pergastrically or intravenously administered type II collagen

Thompson, H. S. G.; Staines, N. A.

doi:10.1007/bf01971237

Cited by 21 publications

(9 citation statements)

References 3 publications

(2 reference statements)

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“…Gliadin is responsible for CD, a condition sustained by an abnormal mucosal T-cell response to gliadin. Herein, we studied the potential for tolerance induction in gluten-free diet mice by administration of whole antigen, as it has been demonstrated that this strategy is effective in a variety of different experimental systems [2][3][4][5][6][7][8]. Our results showed that administration of native gliadin, both i.v.…”

Section: Discussionmentioning

confidence: 99%

“…injection of an antigen before immunization has been shown to represent a potent means to induce Ag-specific peripheral tolerance [3,4,14]. Many studies have reported its potential applicability to the treatment of autoimmune diseases [3,4,[14][15][16][17][18]. Investigation of the cellular mechanisms involved suggests that clonal anergy [5], together with thymic and peripheral T-cell apoptosis [19], are associated with systemic injection of highdose antigen.…”

Section: Discussionmentioning

confidence: 99%

“…injection of antigen in a nonimmunogenic form [1][2][3]. These results have raised the possibility of peripheral tolerance induction as a tool for prevention and/or treatment of ongoing autoimmune diseases.…”

Section: Introductionmentioning

confidence: 99%

“…These results have raised the possibility of peripheral tolerance induction as a tool for prevention and/or treatment of ongoing autoimmune diseases. Given the available results in animal models [2][3][4][5][6][7][8], this approach may prove useful for the treatment of various human organ-specific inflammatory autoimmune diseases when the autoantigens involved are known.…”

Section: Introductionmentioning

confidence: 99%

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Intravenous or Intranasal Administration of Gliadin is Able to Down‐Regulate the Specific Immune Response in Mice

Rossi

Maurano

Caputo³

et al. 1999

Scand J Immunol

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The mucosal lesion in coeliac disease (CD) represents an immunologically mediated injury triggered by gliadin and is restricted by a particular assortment of major histocompatibility complex (MHC) class II genes. Therefore, immunomodulatory strategies to tolerize gliadin‐specific, class II‐restricted T‐cell responses could represent an alternative to current treatments of CD, which are based on a gluten‐free diet. In this study, BALB/c mice derived from a gluten‐free diet colony were tolerized by either intranasal (i.n.) or intravenous (i.v.) administration of single or multiple doses of gliadin. While a single dose failed to induce tolerance, a significant decrease in gliadin‐specific T‐cell proliferation was detected (P < 0.001) after multiple i.n. or i.v. administrations. No significant difference in antibody titre was detected for antigen‐specific immunoglobulin G (IgG) or the IgG1 subclass, but a lower IgG2a‐specific titre was observed. Both interferon‐γ (IFN‐γ) and interleukin (IL)‐2 expression, measured by enzyme‐linked immunosorbent assay (ELISA) and reverse transcription–polymerase chain reaction (RT–PCR), were reduced on antigen administration, both i.v. and i.n. Neither regimen showed a regulatory effect on IL‐4 production. As T helper 1 (Th1) cytokines seem to be important in the pathogenesis of CD, our data therefore highlight the potential of i.n. and i.v. routes for the design of useful immunomodulatory strategies for CD.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Intravenous or Intranasal Administration of Gliadin is Able to Down‐Regulate the Specific Immune Response in Mice

Rossi

Maurano

Caputo³

et al. 1999

Scand J Immunol

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“…[7.8] and intravenous injecencephalomyehtis (EAE) was achteved by feeding an irrelevant tion (i.v.) [9][10][11][12]. Most reported data describe intervention P''""''" ^"^'8^"" ^^'^ '^^'*'*^^ of suppression, medtated by a before immunization.…”

Section: Introdlictionmentioning

confidence: 99%

Suppression of hen egg lysozyme-induced arthritis by intravenous antigen administration: no role in this for antigen-driven bystander suppression

Jacobs

Hoek

Putte

et al. 1994

Clinical and Experimental Immunology

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SUMMARYThe induction of tolerance, particularly by intervention before established immunity, is widely accepted. We studied the effects of intravenous (i.v.) administration of hen egg lysozyme (HEL). before as well as after immunization, on a HEL-induced arthritis. Arthritis and also cartilage destruction were almost completely suppressed when 100 ^i% HEL was injected before immunization. Antigen-specific proliferative T cell responses and IL-2 production in vitro were inhibited. Antigenspecific immunogiobulin and IgGl titres were equal in control and tolerized mice, in contrast to lowered IgG2a litres in tolerized animals. Detailed hisiological studies showed that the immune complex-dependent poiymorphonuclear cell phase {<24 h after arthritis induction) was equal for control and HEL-injected mice. Only in the T cell-dependent phase of the arthritis (> 24 h), did suppression become pronounced in tolerized mice. I.V. administration of 100 ^g HEL after immunization could only marginally reduce infiltrate and exudate. and no reduction of cartilage destruction was seen. An elegant way to interfere in an established immunity can be offered by creation of bystander suppresson. We show that i.v. administration of HEL followed by triggering with HEL, at the moment either of immunization or of arthritis induction., does not reduce a methylated bovine serum albumin (BSA)-arthritis. We conclude that arthritis can be suppressed almost totally when HEL is injected intravenously before immunization. Treatment after immunization is less efTeciivc. The i.v. induced suppression is T cell-mediated and antigen-specific: no bystander suppression circuit can be generated.Keywords tolerance intravenous arthritis antigen-specific antigen-driven bystander suppression

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Oral administration of acetylcholine receptor: Effects on experimental myasthenia gravis

Okumura

McIntosh

Drachman

1994

Annals of Neurology

100

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The abnormality in myasthenia gravis (MG) is a deficiency of acetylcholine receptors (AChRs) at neuromuscular junctions due to an antibody-mediated autoimmune attack. Although immunosuppressive drugs are usually beneficial in MG, they produce generalized suppression of the immune system. Treatment should specifically inhibit the immune response to AChR. Oral administration of an antigen may induce specific tolerance and has recently been tested for treatment of several cell-mediated experimental and human autoimmune diseases. In this study, we investigated the effects of oral administration of AChR in an experimental rat model of MG (EAMG), which is antibody mediated. Lewis rats were fed various doses of purified or unpurified Torpedo AChR, or a control antigen, ovalbumin (OVA). They were then immunized with AChR or OVA. We measured antibody responses to Torpedo AChR or OVA, autoantibody responses to rat AChR, cellular responses, cellular suppressive effects, and clinical status. Our results showed that AChR feeding prevented clinical signs of EAMG. It initially primed, then inhibited, antibody responses to foreign (Torpedo) AChR and self (rat) AChR, with a delayed onset. Cellular responses to AChR, measured by lymphocyte proliferation and interleukin-2 production, were markedly inhibited. The effects were dose dependent. Unpurified AChR given in comparable amounts was far less effective than pure AChR. OVA feeding had similar, but even more potent effects on humoral and cellular immune responses to OVA, but did not inhibit clinical EAMG or AChR responses. Moderate nonspecific suppression by splenic T cells from orally treated animals was demonstrated in vitro. We conclude that oral therapy is beneficial in EAMG and may prove effective in MG patients. Early priming and delayed inhibition suggest that a molecule with less immunogenic potential than intact AChR might be more effective as a therapeutic agent.

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Suppression of collagen-induced arthritis with pergastrically or intravenously administered type II collagen

Cited by 21 publications

References 3 publications

Intravenous or Intranasal Administration of Gliadin is Able to Down‐Regulate the Specific Immune Response in Mice

Intravenous or Intranasal Administration of Gliadin is Able to Down‐Regulate the Specific Immune Response in Mice

Suppression of hen egg lysozyme-induced arthritis by intravenous antigen administration: no role in this for antigen-driven bystander suppression

Oral administration of acetylcholine receptor: Effects on experimental myasthenia gravis

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