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Title:	SLAM Family Receptors and Autoimmunity
Author:	Sintes, Jordi; Bastos, Ricardo; Engel Rocamora, Pablo
Notes:	The immune system is responsible for the defense against a wide array of pathogens but without responding to each individual’s (self) antigens. Autoimmune diseases are characterized by a loss of tolerance to self antigens that leads to the appearance of autoreactive lymphocytes. The main factors that contribute to the development of autoimmunity are genetic susceptibility and infection. Disease susceptibility is the result of the combined action of multiple genes. It has been shown that certain gene polymorphisms can influence the establishment of self-tolerance. The human immune system is a complex machinery involving numerous proteins. Cell-surface proteins expressed by leukocytes are of particular relevance due not only to their participation in the network of interactions that regulate the innate and adaptive immune responses, but also to their potential as excellent targets for diagnostic and therapeutic interventions (Diaz-Ramos et al., 2011). These molecules deliver signals that modulate leukocyte development, activation, survival, clonal expansion, and important effector functions. Some of these cell-surface signaling molecules have the capacity to activate lymphocytes and other leukocytes, while others function as downmodulators of immune responses, playing a key role in the establishment of tolerance to self antigens. Thus, it is not surprising that many of the allelic variants associated with autoimmunity identified, to date, correspond to leukocyte cell-surface molecules (Maier & Hafler, 2009). In this review we will discuss recent observations that point to a key role of signaling lymphocyte activation molecule family (SLAMF) receptors in the development of autoimmunity.
Subject(s):	-Malalties autoimmunitàries -Autoimmune disease
Rights:	cc by (c) Sintes, Jordi et al., 2011 http://creativecommons.org/licenses/by/3.0/es/
Document type:	Book Part Article - Published version
Published by:	IntechOpen
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