LILRA3

PBB GE LILRA3 206881 s at fs

LILRA3 (Leukocyte Immunoglobulin-Like Receptor A3), also known as ILT6 (Immunoglobulin-Like Transcript 6), is a protein that in humans is encoded by the LILRA3 gene. This gene is a member of the leukocyte immunoglobulin-like receptor (LIR) family, which is found within the LILR gene cluster on chromosome 19q13.4. LILRA3 is one of the soluble members of this family, lacking a transmembrane domain, which distinguishes it from its membrane-bound relatives.

Function[edit | edit source]

LILRA3 is involved in the regulation of the immune system. It binds to class I major histocompatibility complex (MHC) molecules on antigen-presenting cells and transmits inhibitory signals that regulate immune responses. The interaction between LILRA3 and MHC class I molecules is critical for the modulation of T cell and natural killer cell activities, playing a role in maintaining immune tolerance and preventing autoimmune responses. However, unlike most LILR family members, LILRA3 does not possess a transmembrane region and is secreted as a soluble protein. Its exact mechanism of action and how it influences immune cell function as a soluble receptor remains an area of active research.

Genetic Variability and Disease Association[edit | edit source]

Variations in the LILRA3 gene have been associated with susceptibility to several autoimmune diseases, including multiple sclerosis (MS), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE). A common deletion polymorphism in the LILRA3 gene leads to the absence of the LILRA3 protein, which has been linked to an increased risk of these diseases. This suggests that LILRA3 may play a protective role in the immune system, and its absence or functional alteration could disrupt immune regulation, leading to autoimmunity.

Research Directions[edit | edit source]

Research on LILRA3 is ongoing, with studies focusing on elucidating its precise role in immune regulation, its potential as a biomarker for autoimmune diseases, and its therapeutic implications. Understanding the mechanisms by which LILRA3 interacts with other components of the immune system, such as its ligands and signaling pathways, could provide new insights into the pathogenesis of autoimmune diseases and lead to novel therapeutic strategies.