REVIEW - The low-throughput protein A adsorber: Hypothesis for mechanism of action in RA.

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Modern Rheumatology

Publisher: Springer Tokyo

Date: February 2005

Pages: 9 - 18

REVIEW ARTICLE

The low-throughput protein A adsorber: an immune modulatory device.

Hypothesis for the mechanism of action in the treatment of rheumatoid

arthritis

Jürgen Brunner1, M. Kern2, Udo S. Gaipl1, E. Munoz1,

Reinhard E. Voll3, Joachim R. Kalden1, Craig W. Wiesenhutter4 and

Herrmann1

(1) Institute for Clinical Immunology, Department of Medicine

III, Friedrich- University of Erlangen-Nuremberg, Glückstrasse 4a,

91054 Erlangen, Germany

(2) Franz von Prümmer Klinik, Akutklinik für Rheumatologie und

Allgemeinkrankenhaus, Bad Brückenau, Germany

(3) IZKF Research Group 2, Nikolaus-Fiebiger Center of

Molecular Medicine, Erlangen, Germany

(4) Coeur dAlene Arthritis Clinic, Coeur dAlene, 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 . 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 bodys scavenging system.

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