Affiliations: [a] Service of Immunology, Complejo Hospitalario de Ciudad Real, Spain | [b] Service of Pharmacy, Hospital Santa Bárbara Puertollano, Spain | [c] Service of Gastroenterology, Hospital Santa Bárbara Puertollano, Spain
Correspondence:
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Corresponding author: José Miguel Urra Ardanaz, Inmunología-Laboratorio, Hospital Alarcos, Avenida Pio XII s/n, 13002, Ciudad Real, Spain. Tel.: +34 926 213444; Fax: +34 926 212290; E-mail: jurra@hnsa.insalud.es.
Abstract: Tumor necrosis factor alpha (TNFα) has been described as a citokine involved in gastrointestinal mucosal inflammation in Crohn's disease. A single infusion of the chimeric mouse/human monoclonal antibody cA2 anti-TNFα has been established as a new therapeutical procedure. The aim of these study was to determine the effect of the monoclonal antibody cA2 on lymphocyte and monocyte TNFα-producing cells. Initially the patient, with severe Crohn's disease (Crohn's disease activity index CDAI > 350), presented a higher number of peripheral blood TNFα-producing cells than healthy controls. The patient received two cA2 treatments throughout one year due the severe activity of the disease. Before treatment the patient had a large number of TNFα producer cells. A dramatic reduction in lymphocyte and monocyte TNFα producing cells, together a clinical remission (CDAI < 150), was shown after the treatments. Four months after the first cA2 treatment, the patient had a clinical response associated with an important increment of TNFα-producing cells that extended increasing until the second cA2 treatment was averaged. These results suggest that the clinical activity of the Crohn's disease correlates with peripheral TNFα-expressing cells. The cA2 antibody, as well as of neutralize soluble TNFα, also removes TNFα-producer cells, which may collaborate with the anti-TNFαactivity of the antibody treatment.
