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E3 ubiquitin ligases and immune tolerance: Targeting the immune synapse from within?

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Book cover The Immune Synapse as a Novel Target for Therapy

Part of the book series: Progress in Inflammation Research ((PIR))

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Abstract

The success of adaptive immunity relies on the ability to eliminate invading pathogens without eliciting responses against the host. Unique antigen receptors are randomly generated and recognize both self and non-self antigens. Therefore, mechanisms of tolerance must be in place to control the activity of self-reactive lymphocytes. Negative selection in the thymus eliminates most of the developing thymocytes that can recognize self antigens 1, whereas mechanisms of peripheral tolerance prevent the surviving self-reactive cells from engaging in responses against self tissues. Self-reactive T cells can be suppressed by regulatory T cells, and also eliminated by clonal deletion or inactivated by a mechanism known as anergy 2. In anergic T cells, T cell receptor (TCR) signaling is blocked, and cells become unresponsive to subsequent stimulation events 35.

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Puga, I., Macian, F. (2008). E3 ubiquitin ligases and immune tolerance: Targeting the immune synapse from within?. In: Graca, L. (eds) The Immune Synapse as a Novel Target for Therapy. Progress in Inflammation Research. Birkhäuser Basel. https://doi.org/10.1007/978-3-7643-8296-4_9

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