“…Afterward, plasmapheresis has started to be used for the treatment or has been used in different disorders as first‐line therapy, primary stand‐alone treatment, or in combination with other therapeutic means, such as thrombotic thrombocytopenic purpura, myasthenia gravis, neuromyelitis optic, multiple sclerosis, Guillain–Barre syndrome, Chronic Inflammatory Demyelinating Polyneuropathy, Goodpasture's syndrome, Rapidly Progressive Glomerulonephritis, systemic vasculitis, immune thrombocytopenica, transplant sensitization, transplant rejection (antibody type), Waldenstrom's macroglobulinemia, and hyperviscosity syndrome [3]. Although the beneficial effects of plasmapheresis have been proven in different human diseases [4–6], full understanding of mechanisms of plasmapheresis action requires further extensive research [7]. Until now, the proposed mechanisms for effects of TPE are [8–10]: (i) removal of the “bad” antibodies; (ii) stimulation of proliferation of B cells and plasma cells, increasing their sensitivity to immunosuppressants; (iii) removal of the immune complexes with enhanced macrophage/monocyte function; (iv) replacement of the missing plasma components; (v) withdrawal of cytokines; (vi) modification of the lymphocyte numbers; (vii) augmented activity of T regulatory and suppressor cell activity; and (viii) correction of T‐helper cell type 1/2 ratio, by favoring Th1 predominance.…”