No Evidence for Generation of Th‐2‐like MBP‐Specific T‐Cell Lines by Blockade of the Costimulatory Molecule B7‐1

The T helper‐1 (Th‐1)/T helper‐2 (Th‐2) paradigm is relevant for the pathogenesis and therapy of multiple sclerosis. In experimental autoimmune encephalomyelitis, a shift towards a Th‐2 immune response serves as treatment of the disease. In the human immune system, the factors which determine and modulate the differentiation of CD4 + T cells into the Th‐1 or Th‐2 phenotype have yet to be elucidated completely. Here, the split‐well approach was used to analyse costimulatory requirements for the generation of myelin basic protein‐specific T‐cell subsets considered to play a major role in the pathogenesis of multiple sclerosis. Myelin basic protein‐specific T‐cell lines were isolated from peripheral blood cells of healthy individuals in the presence or absence of a blockade of the costimulatory molecule B7‐1, previously reported to be involved in the development of Th‐1 cells. T‐helper type was determined by the interferon/interleukin ratio. Blockade of B7‐1 did not increase the number of Th‐2‐like myelin basic protein‐specific T‐cell lines. Thus, these data show no evidence for an influence of B7‐1 blockade on the development of human myelin basic protein‐specific T‐cell subsets. These results have to be taken into account when discussing whether antibody‐mediated B7‐1 blockade might be a suitable therapy in multiple sclerosis, as demonstrated in experimental autoimmune encephalomyelitis.