Transport

Teleologically seen, transport of antigen is a very important feature of the antigen-removing task for antibodies. Antibodies find their way to the waste baskets located in the reticuloendothelial system, mainly in liver, spleen, and lung where the immune complex will be eventually metabolized. With some viruses as antigens, the organ tropism is anticipated because some viruses target liver (hepatitis B and C virus), others the nervous system (measles, herpes, cytomegalo-viruses), others bone marrow and heart
(coxsackie B3, parvovirus P 19) and others joints (rubella, varicella zoster). If the disposal remains incomplete, the target organ becomes subjet to a circulus vitiosus thus becoming a trash removal site: organs which are subject to insufficient immune complex removal by the professional reticuloendothelial system are (in brackets: diagnosis): lung (pneumonia), heart (myocarditis), skin (vasculitides), joint (synovitis). In these cases we all at a sudden find hepatitis viruses in the skin, neurotropic bacteria and viruses in the lung!
A typical consequence of chronically circulating immune complexes is thrombocytopenia, because blood platelets carry Fc-receptors to which immobilized, antibody induced cross-linked Fc fragments of Ig bind. Heparin-induced thrombocytopenia sees heparin first binding to platelets which thus induce anti-heparin-antibody synthesis: the antibody targets directly an antigen on the surface of the platelet. Fortunately, red blood cells (RBCs) are endowed with C3b receptors (CR1/CD35) that will carry immune complexes linked with C3b. RBCs express an average of 90% of the CR1 but among healthy people, the number of CR1 on RBCs varies widely, yet the phenotypic expression regulated by 2 codominant alleles is stable. RBCs are thus transporters of immune complexes and we know that an RBC needs about 2 minutes to transport an immune complex from its site of generation to its site of removal.
Should this system become overloaded then systemic immune complex overload is a logical consequence.

Red blood cells are not solely transporting oxygen!
We here can see that they carry an immune complex according to the depicted scheme (out of scale). A paper appearing in Molecular Medicine by Owuor BO et al: Reduced immune complex binding capacity and increased complement susceptibility of RBCs from children with severe malaria associated anemia, brings this RBC function to the point: deficiencies in RBC CR1 and CD55 in children with severe malaria associated anemia were accompanied by a marked decline in IC binding capacity and increased C3b deposition in vivo and ex vivo
Mol Med 2008;14(3-4):89-97

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