ABSTRACT
I. INTRODUCTION When the hybridoma technique of Kohler and Milstein was introduced in 1975, its potential for clinical use was immediately perceived (I). Within a decade, therapeutic monoclonal antibodies (MAb) directed against the pan-T-cell antigen CD3 became established in clinical use (2). H took longer to exploit the obvious advantage of a subclass-specific antibody for clinical purposes. Though the T-helper-specific human T4 antigen had already been described in 1979, a systemic study of its usefulness as target for immunotherapies became possible only when a MAb against its murine homolog L3T4 was made available (3). Since then, CD4 antibodies have become a major analytical and therapeutic tool to dissect and influence the immune response in vivo. Many studies have revealed the central role of CD4+ T cells in the majority of experimental autoimmune diseases, which could be prevented by early treatment with CD4 MAb. Moreover, already established experimental autoimmune diseases were susceptible to treatment ( 4,5). The effort to introduce CD4 MAb into clinical use was mainly nourished by the expectation of a more selective immunosuppression sparing the T-helper-cell-independent arms of the immune response.
