Immune cytolysis viewed as a stimulatory process of the target.
Humoral and cellular mechanisms of immune cytolysis, as effected by antibody and complement (Ab + C') or by cytolytic T lymphocytes (CTL), have traditionally been considered the end result of early but terminal membrane damage, in turn causing colloid-osmotic lysis of the target cell. A comprehensive theory explaining and relating known prelytic cellular events to subsequent membrane damage is lacking, nor is there a specific picture as to the role and mode of action of Ca2+, which appears to be involved in both complement- and cell-mediated cytolysis (C'MC and CMC, respectively). Recent studies are in support of the view that both Ab + C' and CTL induce a comparable series of prelytic events, in the TC, initiated by membrane depolarization, which in turn bring about voltage-dependent Ca2+ influx or its intracellular release. Persistent elevation of cytosolic Ca2+ can induce massive stimulation of cellular ATPases (actomyosin, Ca2+) and cause exhaustive depletion of ATP. Consequently, Na+-pumping is slowed down and colloid-osmotic lysis ensues. Hence, in our view, membrane damage in immune cytolysis is the result rather than the cause of intracellular events culminating in lysis.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism; D003080:Cold Temperature; D003165:Complement System Proteins / Q000276:immunology; D003600:Cytosol / Q000378:metabolism; D003602:Cytotoxicity, Immunologic; D066298:In Vitro Techniques; D008564:Membrane Potentials; D051379:Mice; D009374:Neoplasms, Experimental / Q000276:immunology / Q000503:physiopathology; D009995:Osmosis; D011188:Potassium / Q000378:metabolism; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology* / Q000502:physiology
D000255:Adenosine Triphosphate; D003165:Complement System Proteins; D011188:Potassium; D002118:Calcium