Abstract
The specific targeting of dendritic cells (DCs) using antigen-delivering antibodies has been established to be a highly efficient protocol for the induction of tolerance and protection from autoimmune processes in experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS), as well as in some other animal disease models. As the specific mechanisms of such induced tolerance are being investigated, the newly gained insights may also possibly help to design effective treatments for patients. Here we review approaches applied for the amelioration of autoimmunity in animal models based on antibody-mediated targeting of self-antigens to DCs. Further, we discuss relevant mechanisms of immunological tolerance that underlie such approaches, and we also offer some future perspectives for the application of similar methods in certain related disease settings such as transplantation.
Highlights
Over one hundred years ago, Paul Ehrlich coined the term “horror autotoxicus” to define an immune attack against an organism’s healthy tissues [1]
Though the non-obese diabetic (NOD) mouse has been the primary animal model of spontaneous type 1 diabetes, important insights were gained from studies using double transgenic mice, in which T cell receptors (TCRs) transgenic CD4+ T cells are specific for hemagglutinin (HA), which is expressed as a neo-self antigen by pancreatic beta cells [102,103,104,105,106]
The induction and modulation of tolerance by targeting dendritic cells (DCs) with antigen-delivering antibodies have proven successful in the amelioration of disease processes in a range of animal models including multiple sclerosis (MS) and diabetes
Summary
Over one hundred years ago, Paul Ehrlich coined the term “horror autotoxicus” to define an immune attack against an organism’s healthy tissues [1]. Tcells (pTreg cells) and areantigens often for antigen immune tolerance to the specific self-antigens and amelioration of autoimmune disease symptom tolerogenic are good inducers of peripheral regulatory. Some DCs can still activate T cells, but this outcome of T cell activation by ntDCs can result in the induction of pTreg cells and tolerance (as discussed above) [21,22,27] These inherent tolerogenic functions provide a very strong rationale for the development of approaches seeking to enhance the antigen-specific immunoregulatory mechanisms mediated by ntDCs that reside in the peripheral immune system and that may remain unaffected by the developing autoimmune process that is limited to a specific site or organ. As reviewed in [61], the administration of DC vaccine formulations employing carriers with specific physical properties (including molecular size, pH, charge, or the inclusion of particular chemokines, cytokines, or adjuvants) can elicit desired tolerogenic or pro-immunogenic responses of DCs in peripheral lymphoid organs (including draining lymph nodes), further work is necessitated to determine which specific carrier properties work best with specific delivery methods and are most appropriate for specific diseases and conditions
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