Complement-component-C3-opsonized immunoglobulin G anti-DNA antibodies do not bind effectively to red blood cells unless aggregated on a high-Mr DNA matrix

Horgan, Carol; Taylor, Ronald P.

doi:10.1042/bj2240755

Cited by 3 publications

(1 citation statement)

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“…showed that Immune complexes bound to both cell types with nearly equal avidity. The high binding constants we observed are consistent with previously published reports [13.28] and support the concept that the immune complex is a large multi-valent ligand which interacts with multiple receptors on the cell surface [28,34]. Despite the similarity in binding iividity.…”

Section: Discussionsupporting

confidence: 92%

Mechanism of transfer of immune complexes from red blood cell CR1 to monocytes

Emlen

Carl

Burdick

1992

Clinical and Experimental Immunology

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SUMMARYComplement receptor I (CRI) oti primate red blood cells (RBC) binds most complement-fixing immune complexes iti the circulation. It has been postulated that by binding them. RBC keep immune complexes in the intravascular space and deliver ihem to the tissue macrophages of the mononuclear phagocyte system. We have developed an in vitro model to study the transfer of RBC-bound immune complexes {heat-aggregated IgG and DNA-anti-DNA) to phagocytic cells (human monocytes).•• Transfer of immune eomplexes from RBC to tnonocytes occurred significantly more rapidly than monocyte uptake of the same immune complexes from solution, ln the transfer process, complexbearing RBC vtcre not bound or sequestered by the monocyles. To define the monocyte receptors involved in binding immune complexes from the RBC surface, monocyte receptors were blocked with MoAbs {anti-CRI, anti-FcRII) or EDTA (to block CR3). Monocyte binding of immune complexes primarily used CRI with a small contribution from FcRlI, and with little or no contribution from CR3 and FcRl. Uptake ofitnmune complexes from solution employed the same monocyte receptors as binding of complexes from the RBC surface. Immune complexes in solution bound to RBC and to monocytes with equally high avidity (approximately I x 10" 1/M), but monocytes expressed a 15-20-foid greater number of immune complex binding sites. We propose thai immune complexes distribute between RBC and monocytes according to the binding capacity of these cells, such that at equal or high RBC/monocyte ratios as would be seen in the circulation immune complexes bind to RBC, but at low RBC/monocyte ratios {as would be seen in the sinusoidal circulation of the liver and spleen), most immune complexes bind to monocytes. To define the pathway by which immune complexes move from RBC to monocytes, their release from RBC CRI was examined. Under various conditions, the dissociation rate was extremely slow, and did not increase with the addition of monocyte supernatants. To examine whether factor I-mediated processing of immune eomplexes enhances binding of immune complexes to monocytes, RBC-bound complexes were released with factor I, and binding of these "processed' immune complexes to monocytes was examined. Monocyle binding of ihese processed immune complexes was slower than o\' control ones; furthermore, performanceof transfer experiments at 4 C, which significantly shows enzymatic processes, did not decrease the rate of immune complex transfer from RBC to monocytes. We conclude that net movement of immune complexes from RBC to monocytes is driven by the greater number of complex-binding sites available on the monocyte relative to the RBC. and that the pathway of transfer of immune complexes from RBC CR 1 to tiionoeytes is not dependent on factor I or other enzymatic processing of immune complexes. The RBC. by virtue of their low itnmune complex binding-capacity, and their ability to present immune complexes in a favourable configuration for monocyte binding, play a unique and critical role in the norma...

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Section: Discussionsupporting

confidence: 92%