The CD4 molecule is expressed on T lymphocytes and acts as a co-receptor for the T-cell receptor (TCR) by direct interaction with the major histocompatibility complex class II molecule on antigen-presenting cells. TCR-independent engagement of the CD4 molecule by monoclonal antibodies leads to T-cell inactivation. Moreover, T-helper cells may contribute directly to cutaneous tissue damage in LE by stimulating both macrophages and cytotoxic T cells. Therefore, specific inhibition of T-helper cells using anti-CD4 was considered as a suitable approach to suppress disease activity (Prinz et al. 1996). Accordingly, in vitro, a recombinant chimeric CD4 monoclonal antibody (cM-T412) was found to block T-helper cell functions such as proliferative response to recall antigens, IL-2 challenge, or allogeneic blood mononuclear cells (Riethmuller et al. 1992). Because of the low toxicity and the lack of immunogenicity, this antibody was chosen for first clinical trials (Riethmuller et al. 1992). Five patients with DLE, including two with systemic involvement, were treated with anti-CD4. The antibody was given in two cycles of seven and four infusions, separated by an interval of 4-7 weeks with a total dose of 275 mg (two patients with DLE) or 400 or 475 mg (one patient with SCLE and two with SLE). After antibody treatment, an immediate improvement in lesional inflammatory activity and healing of cutaneous lesions was observed. Long-lasting improvement with a restoration of responsiveness to conventional anti-inflammatory agents also was noticed. Moreover, proteinuria as an index of lupus nephropathy was fully resolved. The antibody was well tolerated, and side effects such as nausea and diarrhea were controlled by application of metoclo-pramide and loperamide. Further controlled clinical trials are required to prove these very promising but preliminary results.

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