REVIEW ARTICLE
The low-throughput protein A adsorber: an immune modulatory device. Hypothesis for the mechanism of action in the treatment of rheumatoid arthritis
Jurgen Brunner1, Peter M. Kern2, Udo S. Gaipl1, Luis E. Munoz1, Reinhard E. Voll3, Joachim R. Kalden1, Craig W. Wiesenhutter4 and Martin Herrmann1
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| (1) |
Institute for Clinical Immunology, Department of Medicine III, Friedrich-Alexander University of Erlangen-Nuremberg, Gluckstrasse 4a, 91054 Erlangen, Germany |
| (2) |
Franz von Prummer Klinik, Akutklinik fur Rheumatologie und Allgemeinkrankenhaus, Bad Bruckenau, Germany |
| (3) |
IZKF Research Group 2, Nikolaus-Fiebiger Center of Molecular Medicine, Erlangen, Germany |
| (4) |
Coeur d'Alene Arthritis Clinic, Coeur d'Alene, ID, USA |
Abstract To achieve specific removal of pathogenic antibodies (Ab) or immune complexes (IC), several adsorbers have been developed. We discuss the mode of action of low-throughput staphylococcal protein A (SPA) immunoadsorption. The SPA-based Prosorba apheresis is likely to modify some of the autoantibodies (autoAb) or IC. The low-throughput adsorber showed very limited adsorption capacity of circulating autoAb and/or circulating IC. Besides changes of humoral diagnostic parameters, cellular changes could be observed in the Prosorba-treated patients. These changes were rather similar to those that have been observed in a patient successfully treated with Ab against tumor necrosis factor α. We propose an adsorber-catalyzed conversion of small, tissue-penetrating, scarcely detectable, non-complement-binding, proinflammatory IgG-rheumatoid factor (RF)-based IC into the more readily phagocytosed species of IC: intermediate-sized, partially cryoprecipitable, non-tissue penetrating IC that are opsonized with complement. These IC are rather short-lived and could quickly be cleared by the body's scavenging system.
Key words Apheresis - Immunmodulation - Immune complex (IC) - Rheumatoid arthritis (RA) - Staphylococcal protein A (SPA) |