CD4 antibody treatment of severe psoriasis.

Appearance of legs (A) before and (B) 11 days after first CD4 antibody infusion. role in this disorder. Not only the generalised exacerbation of psoriasis but also the chronic psoriatic plaques responded. The nature of the putative, ep~dermis-derived, stimulus-inducing T-cell activation and infiltration remains unknown. efficacy of a rnouse/human chimeric W 4 antibody: functional contributions of isorype and Fc. Trearment of rheumatoid arthritis with monoclonal CD4 antibody M-T151. SlR,-Dr Polzot-Martin and his colleagues (June 15, p 1477) suggest that CD4 monoclonal antibodes and peptide T could be helpful in the treatment of resistant psoriasis. We have lniuated a phase I1 c h d ma1 of a 0 4 monoclonal antlbody m generalised severe psonasls and we report h s treatment m three patients. 'The first patient, a 61-year-old man who had psoriasis vulgaris for 23 years, had a severe psoriahc erythroderrna wrrh a psoriasis area sensinvity mdex (PASI) of 35 a few days before entenng the study. He rece~ved dally 2 h infusions of CD4 antlbody (clone BB14, munne IgG,, 0.2 mg/kg per day) for 8 days. Clinical tolerance was very good, apart from chills dunng the first mfusion. Improvement started on the fourth day of treatment and was greatest at day 30 (PASI, 12). He deteriorated progressively within a 2-month follow-up (PASI, 20). The two other patlents (aged 40 and 32), wlth disease duration of 10 and 13 years, respecuvely, had chronic psonasis (PASI, 15 and 16). Previous treaments, including retinoids and methotrexate, had been withdrawn because of lack of efficacy and/or toxic side-effects. These patients received CD4 antibody (0.8 mg/kg per day for 3 days, then 0.4 mg/kg per day for 5 days). Clinical improvement was observed on day 8 (PASI, 10 and 8, respectively) and was greatest after 34 weeks (PASI, 0 and 4, respectively). In all rhree patients histological examination of healed skin lesions taken at day 30 showed an almost normal appearance of the skin architecture, with some signs of fibrosis but without any epidermal or dermal signs of psoriasis. The pathogenesis of psoriasis is still unclear but recent studies have ernphasised the role of activated CD4 cells infiltrating the lesional skin.'? The therapeutic activity of cyclosporin2 and our results with CD4 monoctonal antibodies support this hypothesis and suggest that CD4 cells may be relevant targets for irnrnunointervention in the most severe forms of this disease. Sl~,-we were surprised by the lnforrnauon put forward by …