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EFFECT OF ANTI-LFA1 (CD11a) MONOCLONAL ANTIBODIES IN ACUTE REJECTION IN HUMAN KIDNEY TRANSPLANTATION

1991; Wolters Kluwer; Volume: 52; Issue: 2 Linguagem: Inglês

10.1097/00007890-199108000-00020

1534-6080

Brigitte Le Mauff, Maryvonne Hourmant, Jean‐Philippe Rougier, M. Hirn, Jacques Dantal, R. Baatard, Diego Cantarovich, Yannick Jacques, Jean Paul Soulillou,

Renal Diseases and Glomerulopathies

A murine IgG1 monoclonal antibody, 25–3 (Immunotech, France), directed against the α chain (CD11a) of the human LFA1 molecule was used in the treatment of 7 histologically documented first acute rejection in first kidney transplantations under cyclosporine. Four patients (group I) received 20 mg/day for 2 days and 10 mg/day for 8 days of 25–3 MoAb. One developed Quincke's edema after the first injection of 25–3 and was immediately withdrawn from the study. In 2 patients, whose serum creatinine continued to increase, 25–3 MoAb was replaced by steroids, followed by ALG after 3 and 4 days of treatment, respectively. In the last case, rejection was reversed by 25–3 MoAb alone. As the clinical response of rejection to 25–3 was poor, another group of 3 patients (group II) was treated with 25–3 at a dose of 40 mg/day for 2 days, 20 mg/day for 2 days, and 10 mg/day for 6 days, but 25–3 was still unsuccessful in reversing acute rejection, and rescue treatment was initiated between days 5 and 8 in all cases. MoAb tolerance was excellent in 3 patients. With the exception of the one case of Quincke's edema, only minor side effects were noted in the last 3 recipients. 25–3 MoAb serum trough levels peaked between 1.5–3.5 μg/ml at day 3 in group I and between 2–9 μg/L at day 2 in group II. Surprisingly, only one patient, in group I, exhibited a borderline IgG immune response against 25–3. These findings suggest that the 25–3 anti-CD11a MoAb is ineffective in controlling the course of acute rejection in kidney transplantation. However as already reported for another anti-LFA1 or with an anti-CD4 MoAb in mouse, 25–3 would be the first example in humans of a MoAb that does not elicit a strong immune response against its own determinants. This property might have important applications if 25–3 can prevent rejection in a prophylactic protocol or block the immune response against other MoAbs.