Description:
<jats:title>Abstract</jats:title><jats:p> <jats:italic>Background</jats:italic>. Immunologic abnormalities seem to play an important role in systemic sclerosis (SSc).</jats:p><jats:p> <jats:italic>Methods</jats:italic>. We studied the following immune parameters to get more insight into SSc: autoantibodies (antinuclear antibodies (<jats:sc>ana</jats:sc>), anti‐Scl‐70, anticentromere antibodies (<jats:sc>aca</jats:sc>) subsets of lymphocyte subpopulations and markers of their activation, as well as serum levels of <jats:sc>il</jats:sc>‐2, the soluble <jats:sc>il</jats:sc>‐2 receptor (<jats:sc>sil</jats:sc>‐2<jats:sc>r</jats:sc>), <jats:sc>il</jats:sc>‐6 and its correlation to N‐terminal procollagen‐Ill propeptide (<jats:sc>p</jats:sc><jats:sc>iii</jats:sc><jats:sc>p</jats:sc>), and finally, the <jats:sc>il</jats:sc>‐6 production by SSc and normal dermal fibroblasts.</jats:p><jats:p> <jats:italic>Results</jats:italic>. In patients with active SSc, we found a reduced number of <jats:sc>cd</jats:sc>2+ T‐lymphocytes and an increase in the expression of T‐lymphocyte activation markers such as <jats:sc>cd</jats:sc>25+ and <jats:sc>cd</jats:sc>71+, <jats:sc>hla</jats:sc>‐<jats:sc>dr</jats:sc> la, as well as elevated serum levels of <jats:sc>sil</jats:sc>‐2<jats:sc>lr</jats:sc> and <jats:sc>il</jats:sc>‐6. SSc fibroblasts did not produce more <jats:sc>il</jats:sc>‐6 than normal fibroblasts in monolayer cultures.</jats:p><jats:p> <jats:italic>Conclusions</jats:italic>. Our data show that a wide range of immunologic parameters are altered in SSc. In general, T‐helper (<jats:sc>th</jats:sc>) lymphocytes are activated possibly because of reduced T‐suppressor (<jats:sc>ts</jats:sc>) and natural killer (<jats:sc>nk</jats:sc>)‐cell levels, TH may polyclonally stimulate B cells, which in turn produce higher amounts of autoantibodies. Our findings support the concept that TH cell‐derived cytokines/growth factors stimulate matrix protein synthesis by fibroblasts, resulting in generalized fibrosis.</jats:p>