Human CD8(+) T cells and NK cells express and secrete S100B upon stimulation.

Previous studies have demonstrated the utility of S100B as a surrogate marker of brain-related pathologies, e.g. neuropsychiatric disorders, and melanoma progression, which have an inflammatory component. This study addresses the relevance of S100B(+) lymphocytes in mediating such responses. S100B expression was determined in human peripheral blood leukocytes isolated from healthy volunteers using flow cytometry. S100B(+) lymphocytes were characterised for phenotype, cytokine production and S100B secretion. In addition, we investigated whether S100B activates monocytes and neutrophils. S100B(+) cells comprised 2-4% of all lymphocytes and the majority displayed a CD3(+) CD8(+) phenotype; fewer cells were CD3(-) CD56(+) NK lymphocytes. Comparison of S100B(+) and S100B(-) CD3(+) CD8(+) cells revealed no differences in production of interferon gamma (IFNγ) and interleukin-2 (IL-2). Stimulation of S100B(+) CD3(+) CD8(+) lymphocytes with anti-CD3 or phytohaemagglutinin resulted in release of S100B. High concentrations of recombinant human S100B triggered upregulation of CD11b and membrane shedding of CD62L in granulocytes and monocytes. These findings set the stage for a new field of research addressing a S100B-mediated crosstalk between the innate and adaptive immune systems if close proximity of effector and responder cells accomplishes sufficient local S100B levels. In various physiological and pathological conditions S100B might function as an interface to immunological processes, distinct from known cytokine- and chemokine-mediated pathways.