Titlebook: Cytotoxic Effector Mechanisms; Eckhard R. Podack Conference proceedings 1989 The Editor(s) (if applicable) and The Author(s), under exclus

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書目名稱Cytotoxic Effector Mechanisms讀者反饋學(xué)科排名

Herbivorous

Structure and Function of C8 in the Membrane Attack Sequence of Complement,es per complex differs depending on C9 input and conditions of formation. The ultrastructure varies accordingly from what are functional lesions with one or a few C9s to highly organized porelike structures formed by polymerization of as many as 16 C9s per C5b-8. Facts and controversies about the fu

ORE

Granzymes: a Family of Serine Proteases in Granules of Cytolytic T Lymphocytes, (. and . 1980; . et al. 1981, 1984), further implicating the involvement of proteases in the cytotoxic event. While pretreatment of the effector cell with protease inhibitors has no effect on the lytic activity of NK cells, cytotoxicity is highly sensitive to the presence of inhibitors for a short

Morbid

Cougar

A Serine Protease-Encoding Gene That Marks Activated Cytotoxic T Cells In Vivo and In Vitro,enotype to imply function is that these markers are expressed on both active and resting T cells. Thus, they cannot be used to distinguish between the cells participating in a localized immune response and those nonspecifically present at the site. To identify cytotoxic lymphocytes more accurately,

試驗

Structure and Function of the Family of Proteoglycans That Reside in the Secretory Granules of Natu (BMMC) (. et al. 1982; . et al. 1985), and rat basophilic leukemia-1 (RBL-1) cells (. et al. 1980b; . et al. 1985). Human (. et al. 1985) and mouse (. et al. 1983) natural killer (NK) cells and rat large granular lymphocyte (LGL) tumor cells (. et al. 1987) synthesize cell-associated chondroitin su

試驗

https://doi.org/10.1007/978-0-230-62944-8he mechanism of complement-mediated cytolysis (for review, see . 1986; . and . 1984). Because the effector molecule of cytotoxic lymphocytes seemed to perforate the target membrane, it was designated “perforin 1” or “P1” (. and . 1983). The assembly of P1 into transmembrane tubules resembles the for

法律

Clinical Features of Aplastic Anaemiaes per complex differs depending on C9 input and conditions of formation. The ultrastructure varies accordingly from what are functional lesions with one or a few C9s to highly organized porelike structures formed by polymerization of as many as 16 C9s per C5b-8. Facts and controversies about the fu

鬼魂

Expiration

Clinical Features of Aplastic Anaemiacylindrical structures with similar dimensions (. et al. 1982 a), a natural conclusion is that complement lysis is caused by the ability of C9 to insert and polymerise within the bilayer to form hollow pore complexes. An alternative to the pore model postulates that C9 causes lysis by a detergent-li