Theoretical Background of Effect Mechanism by Extracorporeal Immunomodulation

Abstract

Therapeutic plasmapheresis has usually been applied to diseases with unknown causes. Clear analysis of the mechanism of the effect that apheresis has on diseases derived from unknown causes has not been completed. The effect of leukocytapheresis on ulcerative colitis (UC) or rheumatoid arthritis (RA) also lacks clear analysis, but removal of 10(10) adhesive cells resulted in the suppression of both acute and chronic inflammatory reactions. The number of cells removed was not unreasonable for efficacy. A quite acceptable explanation is that the cells activated in the inflammatory lesions are more adhesive than nonactivated cells. However, only a few minutes of contact with the surface of the device can activate blood immune cells. All of the apheresis therapies, not only leukocytapheresis, should be evaluated for their efficacies, excluding the effects of contact activation. According to results presently available, the suppressive effect of leukocytapheresis on RA or UC is through to depend upon the removal of activated inflammation related cells that might transfer inflammatory signals. It may be that those cells removed are bound because of cell stimulation caused by microorganisms or foreign bodies.

Rapid reduction of hepatitis C virus‐Core protein in the peripheral blood improve the immunological response in chronic hepatitis C patients

“…The mechanisms of the favorable effects for CHC patients might not be only the reduction of HCV particles but also the reduction of LDL‐cholesterol and unknown effects of DFPP including that of immune systems as previously reported 5–10 . Plasmapheresis has been used in some T cell‐dependent disorders, such as multiple sclerosis and ulcerative colitis 11–16 . One report indicated that DFPP could directly affect the distribution of lymphocyte subsets 5 …”

Synchronic Intensive Program Therapy of Patients With Rheumatoid Arthritis

“…Такая волна обострения заболевания обычно связана с развитием синдрома рикоше та [15,23,25], возникающим в результате увели чения продукции аутоантител в ответ на эксфу-зию из циркуляции большого пула иммуногло булинов [6,28].…”

“…Так, плазмаферез способствовал подавлению системных прояв лений РА, которые обычно обусловлены имму-нокомплексным васкулитом , путем выведения из циркуляции ЦИК [28,29], в то время как пульс-терапия метотрексатом и введение метип реда подавляли выработку антител, снижали активность лимфоидных клеток. В то же время изолированное применение кортикостероидов и цитостатиков в высоких дозах вызывает хоро ший, но также непродолжительный эффект [5, 9, 11].…”