Anti-Ids in Allergy: Timeliness of a Classic Concept

Wallmann, Julia; Pali‐Schöll, Isabella; Jensen‐Jarolim, Erika

doi:10.1097/wox.0b013e3181e61ebf

Cited by 11 publications

(16 citation statements)

References 60 publications

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“…This would be in contrast to our findings with mimotopes from random peptide libraries which were devoid of T-cell stimulatory capacities [26,27]. It is even conceivable that they directly activate T-cells as it has been repeatedly demonstrated that B- and T-cell receptors may share the same idiotypes [6,9]. These aspects should be addressed in future functional studies.…”

Section: Discussioncontrasting

confidence: 81%

“…Therefore, mimotope vaccines usually lack T-cell epitopes [26,27] and thus may be advantageous when inflammation caused by activation of allergen-specific T-cells has to be avoided [37]. Mimotopes can be readily selected from phage display libraries presenting peptides, Fab-fragments or hairpin libraries by screening them with antigen specific antibodies (reviewed by [6]).…”

Section: Discussionmentioning

confidence: 99%

“…In allergy, anti-idiotypic antibodies may adapt opposing functions by enhancing or inhibiting the IgE-mediated response [6]. Anti-idiotypic specificities may bind to B-cell receptors and counter-regulate B-lymphocyte function [7], or to FcεRI-bound IgE and thereby enhance [8] or inhibit the effector phase of type I allergy, and, interestingly, antiidiotypic specificities may be directed against the T-cell receptors of allergen-specific T-lymphocytes [9].…”

Section: Introductionmentioning

confidence: 99%

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Anti-idiotypic Fab Fragments Image a Conserved N-terminal Epitope Patch of Grass Pollen Allergen Phl p 1

Lukschal

Fuhrmann²,

Sobanov

et al. 2011

TOALLJ

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Background and Aims Naturally occurring anti-idiotypic antibodies structurally mimic the original antibody epitope. Anti-idiotypes, therefore, are interesting tools for the portrayal of conformational B-cell epitopes of allergens. In this study we used this strategy particularly for major timothy grass pollen (Phleum pratense) allergen Phl p 1. Methods and Results We used a combinatorial phage display library constructed from the peripheral IgG repertoire of a grass pollen allergic patient which was supposed to contain anti-idiotypic Fab specificities. Using purified anti-Phl p 1 IgG for biopanning, several Fab displaying phage clones could be isolated. 100 amplified colonies were screened for their binding capacity to anti-Phl p 1-specific antibodies, finally resulting in four distinct Fab clones according to sequence analysis. Interestingly, heavy chains of all clones derived from the same germ line sequence and showed high homology in their CDRs. Projecting their sequence information on the surface of the natural allergen Phl p 1 (PDB ID: 1N10) indicated matches on the N-terminal domain of the homo-dimeric allergen, including the bridging region between the two monomers. The resulting epitope patches were formed by spatially distant sections of the primary allergen sequence. Conclusion In this study we report that anti-idiotypic specificities towards anti-Phl p 1 IgG, selected from a Fab library of a grass pollen allergic patient, mimic a conformational epitope patch being distinct from a previously reported IgE epitope area.

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Section: Discussioncontrasting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Anti-idiotypic Fab Fragments Image a Conserved N-terminal Epitope Patch of Grass Pollen Allergen Phl p 1

Lukschal

Fuhrmann²,

Sobanov

et al. 2011

TOALLJ

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“…This finding suggests that immunoglobulin could be the specific blood component mediating the therapeutic efficacy of ABT in patients with AD. Induction of an anti-idiotype immune response (immune response to the antigen-binding portion of immunoglobulin) has long been suggested as the main mechanism of the development of immune tolerance in allergic and autoimmune diseases [18,19]. The possibility of involvement of an anti-idiotype mechanism in the development of the therapeutic efficacy of ABT or AHPT should be further evaluated in future studies.…”

Section: Discussionmentioning

confidence: 99%

Clinical Efficacy of Autologous Plasma Therapy for Atopic Dermatitis

Cho¹,

Kim²,

Kim³

et al. 2013

Dermatology

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Background: The clinical efficacy of autologous blood therapy (ABT) in patients with atopic dermatitis (AD) was demonstrated by a randomized double-blind placebo-controlled study. To characterize the blood component mediating the therapeutic efficacy of ABT for AD, we evaluated the clinical efficacy of autologous plasma therapy (APT) and autologous high-molecular-weight plasma protein fraction therapy (AHPT) in patients with AD in this study. Methods: A total of 22 patients with recalcitrant AD were treated with 8 weekly intramuscular injections of either autologous plasma (n = 11) or autologous high-molecular-weight plasma protein fraction (n = 11) for 7 weeks. Results: The clinical severity score of AD (SCORAD value) of11 patients who completed AHPT significantly decreased from 79.7 ± 17.0 (mean ± SD) at baseline to 65.8 ± 16.4 at 6 weeks and 60.1 ± 16.0 at 7 weeks (Wilcoxon signed-rank test, p < 0.05). There were no significant differences among the SCORAD values measured at baseline (74.2 ± 19.6), at 6 weeks (66.3 ± 23.6) and at 7 weeks (67.5 ± 20.8) in 10 patients who completed APT (p > 0.05). Conclusion: This result suggests that the blood component mediating the therapeutic efficacy of ABT in patients with AD might be present in the high-molecular-weight plasma protein fraction.

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“…In addition to neutralizing secreted antibody, anti-Id can also down-regulate the secretion of the idiotypic antibody [31,32]. This effect is only observed at high concentrations of anti-Id.…”

Section: Anti-id In the Idiotypic Networkmentioning

confidence: 99%

Protective role of anti-idiotypic antibodies in autoimmunity – Lessons for type 1 diabetes

Hampe

2012

Autoimmunity

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Circulating autoantibodies to beta cell antigens are present in the majority of patients with Type 1 diabetes. These autoantibodies can be detected before and at time of clinical diagnosis of disease. Although the role of autoantibodies in the pathogenesis of the disease is debated, their presence indicates a dysregulation of the humoral immune response. Mechanisms regulating autoantibodies in Type 1 diabetes are not well understood. In contrast, in other autoimmune diseases there is acceptance that autoantibodies are regulated not only by antigen but also by other antibodies that bind to the antigen-binding site of these autoantibodies (anti-idiotypic antibodies). The proposed purpose of this network is to maintain an equilibrium between autoantibodies and their anti-idiotypic antibodies, preventing autoimmunity, while allowing a robust response to exogenous antigen. Anti-idiotypic antibodies regulate both autoantibody binding and their levels by a) neutralizing autoantibodies, and b) inhibiting the secretion of autoantibodies. Because it has been proposed that the B lymphocytes that produce autoantibodies function as autoantigen presenting cells, inhibiting their binding to autoantigen by anti-idiotypic antibodies may prevent development of autoimmune disease. This hypothesis is supported by the presence of anti-idiotypic antibodies in healthy individuals and in patients in remission from autoimmune diseases, and by the lack of anti-idiotypic antibodies during active disease. We recently reported the presence of autoantibodies to glutamate decarboxylase in the majority of healthy individuals, where their binding to autoantigen is prevented by anti-idiotypic antibodies. These anti-idiotypic antibodies are absent at clinical diagnosis of Type 1 diabetes, revealing the presence of autoantibodies. Type 1 diabetes (T1D) is an autoimmune disease characterized by the dysfunction and destruction of insulin-producing beta cells by autoreactive T cells. Although much progress has been made towards understanding the respective roles of effector and regulatory T cells in this beta cell destruction, the development of autoantibodies to beta cell proteins is widely considered simply a by-product of the autoimmune destruction of the beta cells, rather than having an active role in the pathogenesis. This view is starting to change based on increasing recognition that autoantibodies can have defined roles in other autoimmune diseases, and the emergence of new data on their role in T1D. This exploration of the role of autoantibodies in autoimmune disease has been spurred, in part, by increasing recognition that development of autoimmune diseases is influenced by regulatory antibodies (anti-idiotypic antibodies) directed against the unique binding site of autoantibodies. This review provides an overview of the development and function of these anti-idiotypic antibodies, and present evidence supporting their role in the development of autoimmune diseases. Finally, we conclude this review with a model of the events that may cause ...

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Anti-Ids in Allergy: Timeliness of a Classic Concept

Cited by 11 publications

References 60 publications

Anti-idiotypic Fab Fragments Image a Conserved N-terminal Epitope Patch of Grass Pollen Allergen Phl p 1

Anti-idiotypic Fab Fragments Image a Conserved N-terminal Epitope Patch of Grass Pollen Allergen Phl p 1

Clinical Efficacy of Autologous Plasma Therapy for Atopic Dermatitis

Protective role of anti-idiotypic antibodies in autoimmunity – Lessons for type 1 diabetes

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