Paradoxically, high doses of Immunoglobulin G from pooled human sera have been used intravenously for treatment of some chronic inflammatory diseases (Newburger JW et al. N Engl J Med 3 15:341, 1986; Ronda N et al. Vox Sang 64:65, 1993), presumably based on its complement attenuating properties (Lutz HU et al. Blood 88:184, 1996; Lutz HU et al. Blood 103:465, 2004). Band 3 modifications likely to occur during RBC ageing enhance membrane affinity for normally circulating antiband 3 antibodies and bring about limited complement activation (Arese P et al. Cell Physiol Biochem 16:133, 2005). I wonder if autologous IgG is at a high enough concentration in normal serum that it may attenuate complement activity in spite of potential amplification of the immune senescence response during erythrocyte ageing. I would greatly appreciate comments on the subject.
Hi Pedro
Rather than autologous IgG, numerous C' regulatory molecules have a greater role in maintaining hemostasis. Cell surface receptors, such as CD35, CD46, CD55, CD59... Plasma proteins, such as Factor H, CFHR1, C4BP, properdin,.... Erythrocytes express CD55 and CD59, which protect them from C' attack.
Hope this adds to the topic.
Regards, Rosemary
Hi, Dr. Romero,
I don't have exact experimental proof, it is just an odd - and yet unfollowed - side-result, but when You try to determinate the blood group of a sample in the presence of the blood plasma, and You use a huge volume of anti-AB0 antibodies, there is no (or not so fast) haemolysis, meanvhile there is a detecable and relatively fast haemolysis in the presence of samall amount of anti-AB0 Ig-s. (Of course, only when the anti-AB0 reacts with the AB0 antigenes.)
Regards: Csaba
Dear Csaba,
An interesting observation. Many thanks for sharing it. Regards. Pedro.
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