Abstract
The signalling lymphocyte activation molecule (SLAM) family receptors play important roles in modulating immune responses. Previous studies in murine models and patients have suggested an association of the SLAM family (SLAMF) members with the development of autoimmunity, particularly systemic lupus erythematosus (SLE). Since previous investigations on CD244 expression have focussed on NK and T cells, the aim of this study was to evaluate the surface expression of major SLAMF members across monocytes and polymorphonuclear cells in an Asian SLE cohort and explore their potential associations with SLE-related disease activity and autoantibodies. Thirty-nine SLE patients and twenty-nine healthy controls (HC) were evaluated for the expression of CD150, CD84, CD229, CD48, CD244, CD352 and CD319. We determined a significantly lower expression of CD244 on monocytes in SLE patients compared to HC. Furthermore, monocyte CD244 expression was negatively associated with several serum autoantibody titres. Our findings suggest that this molecule plays an important role in immune tolerance mechanisms and should be investigated further.
Highlights
Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder affecting predominantly females of childbearing age and characterised by the development of autoantibodies to nuclear antigens [1, 2]
Cell surface expression of CD229 and CD150 on circulating myeloid cells was undetected in both patients and healthy controls (HC), potentially reflecting restricted expression on natural killer (NK) cells, lymphocytes and antigen presenting cells (APCs) [13, 17, 18]
We have demonstrated a significant reduction in CD244 expression on SLE patient monocytes and platelets compared to gender- and ethnicity-matched healthy subjects in an Asian cohort
Summary
Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder affecting predominantly females of childbearing age and characterised by the development of autoantibodies to nuclear antigens [1, 2]. Antinuclear antibodies (ANAs) form immune complexes with self-reactive material which deposit in tissues and promote infiltration leading to tissue destruction [3] Both genetic and environmental factors have been implicated in SLE onset, with a syntenic region on chromosome 1 in humans and mouse models of lupus. In lupus-prone mice, the Sle1b locus on chromosome 1 mediates loss of tolerance and the development of highly penetrant ANAs [4]. This region encodes the highly polymorphic signalling lymphocytic activation molecule (SLAM) family genes and, in humans, the cluster of SLAM family genes are located within the 1q23 region linked to SLE susceptibility [5, 6]
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