Topic
Lysis
About: Lysis is a research topic. Over the lifetime, 6072 publications have been published within this topic receiving 216978 citations.
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TL;DR: A mathematical model for osmotic fragility of infected cells based on diffusional uptake via PESAC and the two-compartment geometry of infected RBCs is developed and produced permeability coefficients that match both previous isotope flux and patch-clamp estimates.
66 citations
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TL;DR: This paper characterized contact-independent cytotoxicity using the red blood cell as a cellular model and found that the protozoan, under triggering conditions, is able to release molecules that lead to lysis without direct contact between parasite and target cells as a prerequisite.
66 citations
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TL;DR: It is suggested that the LFA‐I/ICAM‐I interaction co‐activates CD3/TCR‐mediated lysis by CTL through both an enhanced CTL‐target cell binding and the delivery of post‐conjugate costimulatory signals.
Abstract:
The primary activation pathway of T cells is via the T-cell receptor (TCR)/CD3 complex, which is functionally interrelated with various accessory molecules. We examined the contribution of the lymphocyte-function-associated antigenI/intercellular adhesion molecule I (LFA-I/ICAM-I) interaction to CD3/TCR-mediated lysis by cytotoxic T lymphocytes (CTL). We used ICAM-I-or+ tumor cell lines as target cells and anti-CD3- or anti-LFA-I containing hetero-cross-linked monoclonal antibody (MAb) to bridge CTL and target cells and simultaneously to activate CTL. The ICAM-I- melanoma-derived cell line lgR39 was relatively resistant to CD3-mediated lysis by both TCRαβ+ and TCRγdL+ CTL, when compared with ICAM-I+ cell lines. Induction of ICAM-I on the membrane of lgR39 cells by tumor necrosis factor (TNF) rendered these cells more susceptible to CD3-mediated lysis. Anti-ICAM-I MAb inhibited this TNF-enhanced susceptibility to lysis, directly demonstrating that the induction of ICAM-I was critical in the TNF-induced increase in susceptibility to lysis of lgR39 cells. CTL formed less efficient conjugates with the ICAM-I- cells as compared to ICAM-I+ cells. Both spontaneous and CD3-induced conjugate formation as well as CD3-mediated lysis of ICAM-I- tumor cells by CTL were enhanced by the addition of anti-LFA-I containing heterocross-linked MAb, thereby mimicking the LFA-I/ICAM-I interaction between CTL and target cells. Soluble anti-CD18 MAb inhibited CD3-mediated lysis of ICAM-I- target cells by CTL without affecting their conjugate formation. Anti-LFA-I MAb added after conjugate formation still inhibited lysis of both ICAM-I+or- tumor cells. Taken together, these findings suggest that the LFA-I/ICAM-I interaction co-activates CD3/TCR-mediated lysis by CTL through both an enhanced CTL-target cell binding and the delivery of post-conjugate costimulatory signals.
66 citations
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TL;DR: The time course of lysis of protoplasts of Micrococcus lysodeikticus was studied by spectrophotometric methods and it was concluded that the cationic detergents act on the complex phosphatidic acid lipid component of the protoplast membrane and that lysis results from secondary osmotic effects.
Abstract: SUMMARY: The time course of lysis of protoplasts of Micrococcus lysodeikticus was studied by spectrophotometric methods. The lytic agents used were sodium dodecylsulphate and a range of cationic detergents which each possessed a n-C12 alkyl chain and comprised the amine hydrochloride, the trimethylammonium bromide, the pyridinium bromide and the quinolinium bromide. Also the inhibition of lysis by uranyl ions and the action of detergents on isolated protoplast membranes were investigated. It is concluded that the cationic detergents act on the complex phosphatidic acid lipid component of the protoplast membrane and that lysis results from secondary osmotic effects. Access to the reactive site by agents of similar hydrophilic-hydrophobic balance is controlled by steric factors. Anionic detergents, however, cause direct disintegration of the protoplast, membrane independent of osmotic stresses, probably by interaction with the membrane protein moiety; a concurrent interaction with lipid, possibly through a lipoprotein complex, is not definitely excluded.
66 citations
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TL;DR: Evidence is presented, indicating that (a) lysophosphatides bind to cells below their critical micelle concentration, (b) micelles themselves are not generally necessary for cell lysis, and the hypothesis that cellular sensitivity to lysolecithin lysis may be determined by the degree of segregation of lysoleCithin-rich areas within the membrane lipid phase is confirmed.
66 citations