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SLAM Family Receptors and Autoimmunity
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Abstract
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.
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SINTES, Jordi, BASTOS, Ricardo and ENGEL ROCAMORA, Pablo. SLAM Family Receptors and Autoimmunity. Chapter 3 in: Mavragani. Clio. 2011. Autoimmune Disorders: Pathogenetic Aspects. ISBN: 978-953-51-6537-8. DOI: 10.5772/802. pp: 53-72. [consulted: 7 of October of 2026]. Available at: https://hdl.handle.net/2445/174341