Abstract
Signaling through coinhibitory receptors downregulates the immune response to prevent excessive immune activation and maintain optimal immunity and tolerance. The aim of this study was to examine the levels of the soluble forms of coinhibitory receptors and their ligands, namely, galectin-9 (the ligand of T-cell immunoglobulin and mucin domain 3) and CD155 (the ligand of T cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain), and their association with clinical features in patients with systemic sclerosis (SSc). The serum levels of galectin-9 and soluble sCD155 were examined by enzyme-linked immunosorbent assays in patients with SSc, and the results were evaluated with respect to clinical features. Patients with SSc exhibited raised serum levels of galectin-9, but not sCD155. Serum galectin-9 levels were raised not only in patients with diffuse cutaneous SSc but also in patients with limited cutaneous SSc. Furthermore, serum galectin-9 levels correlated positively with the erythrocyte sedimentation rate. In addition, increased serum galectin-9 levels tended to be associated with higher mortality and serious organ involvement. These results suggest that galectin-9, but not CD155, may be involved in the pathogenesis of SSc. In addition, the measurement of serum galectin-9 levels could be used to predict serious organ involvement and high mortality in patients with SSc.
Highlights
Systemic sclerosis (SSc) is a generalized connective tissue disorder of unknown etiology and is characterized by excessive fibrosis and microvascular damage in the skin and various internal organs
There was no significant difference in serum galectin-9 levels between patients with diffuse cutaneous SSc (dcSSc) and patients with limited cutaneous SSc (lcSSc)
Increased serum galectin-9 levels tended to be associated with higher mortality and serious organ involvement
Summary
Systemic sclerosis (SSc) is a generalized connective tissue disorder of unknown etiology and is characterized by excessive fibrosis and microvascular damage in the skin and various internal organs. Cutaneous mononuclear cells that infiltrate early SSc skin lesions consist of mostly activated T cells [2]; the degree of cell infiltration correlates with the severity of skin thickening [3]. These infiltrating cells are suggested to release various cytokines, chemokines, or growth factors that play an important role in the initiation and development of fibrosis in SSc [4]. Multiple soluble forms of coinhibitory receptors, including cytotoxic T lymphocyte-associated antigen 4, programmed death-1, and T-cell immunoglobulin and mucin domain 3 (TIM-3), have been demonstrated to play a role in the pathogenesis of SSc [11,12,13]. We examined the levels of serum galectin-9 and soluble sCD155 in Journal of Immunology Research patients with SSc and evaluated the results with respect to clinical features
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