New Antigen-Specific Strategies for Prophylaxis and Treatment of Immune-Mediated Diseases

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About this Research Topic

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Background

The development of safe and effective antigen-specific therapies is needed to treat patients with immune-mediated diseases. These therapies aim at inducing specific tolerization of self-reactive immune cells without altering host immunity to infectious agents. Although advances have been made in the development of efficient antigen-specific therapies, translating these therapies from bench to bedside has remained difficult. This Research Topic aims at focusing on recent advances in our understanding of antigen-specific therapies for the treatment and prophylaxis of allergy, autoimmune diseases and cancer.

Allergen-specific immunotherapy (AIT) is an allergen-specific form of treatment for patients suffering from immunoglobulin E (IgE)-associated allergy. AIT is based on the administration of the disease-causing allergen to induce a protective immunity consisting of allergen-specific blocking IgG antibodies and alterations of the cellular immune response to induce tolerance. Other major advantages of AIT include long-lasting protection induced by AIT and the prevention of disease progression into severe manifestations.

Presentation of antigens on the antigen-presenting cell (APC) surface plays one of the main roles in the development of autoimmune diseases and can thus be a target in the context of antigen-specific therapies. The central functional element of the presentation process is the major histocompatibility complex class II (MHC II). MHC II performs one of the most important functions in the adaptive immune response to foreign pathogens, presenting antigenic peptides on the cell surface. To date, the molecular mechanisms of the antigen presentation in health and disease, are poorly understood. Here, we will focus on three important issues, (i) peculiarities of HLA-DR and -DM interaction; (ii) functioning and modulation of the activity of major antigen processing machines – proteasomes; (iii) induction of regulatory lymphocytes by specific immunotherapy (SIT) and diversity of their surface receptors.

Naturally occurring and SIT-induced regulatory T and B lymphocytes are intensively studied, nonetheless, molecular mechanisms underlying their functioning are still enigmatic. Regulatory functions of B lymphocytes play an important role in the development and suppression of the immune response. Previously it has been demonstrated that B regulatory cells lesion or decrease of its anti-inflammatory activity can lead to a number of immunological pathologies including autoimmune diseases. Though disturbance in BCR development leads to the violation in Breg maturation, more studies on Breg specificity and its BCR structure should be conducted. Therefore, revealing of antigen specificity for sub-population of regulatory lymphocytes in autoimmune abnormalities can contribute to the development of new targeted SIT directly affecting the suppressive immune cells.

We welcome the submission of Original Research, Review, and Method articles, with the aim of giving a comprehensive picture of the new antigen-specific strategies for prophylaxis and treatment of allergy, autoimmune diseases, and cancer. We particularly welcome studies focusing on:

1. New insights on AIT, state of the art AIT as well as new technical solutions through molecular allergology, and the use of AIT for prophylactic application
2. Peculiarities of HLA-DR and -DM interaction in terms of the functioning of antigen-presentation machinery
3. Low molecular weight inhibitors of major antigen processing sub-molecular complexes
4. Structure and specificity of BCRs carried by B regulatory cells
5. New routes of antigen delivery in SIT

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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