Titlebook: Mechanisms of Lymphocyte Activation and Immune Regulation VII; Molecular Determinan Sudhir Gupta,Alan Sher,Rafi Ahmed Book 1998 The Editor(

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書目名稱Mechanisms of Lymphocyte Activation and Immune Regulation VII影響因子(影響力)




書目名稱Mechanisms of Lymphocyte Activation and Immune Regulation VII影響因子(影響力)學(xué)科排名




書目名稱Mechanisms of Lymphocyte Activation and Immune Regulation VII網(wǎng)絡(luò)公開度




書目名稱Mechanisms of Lymphocyte Activation and Immune Regulation VII網(wǎng)絡(luò)公開度學(xué)科排名




書目名稱Mechanisms of Lymphocyte Activation and Immune Regulation VII被引頻次




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Activating and Inhibitory NK Cell Receptorsposed a unique mechanism of immune surveillance for ‘missing self’ (1). The molecular mechanism responsible for this phenomenon has been defined by the identification of membrane receptors on NK cells that bind to MHC class I on potential target cells. While the NK cell receptors initiating a cell-m

Concrete

Regulation of Immune Responses by Inhibitory Receptors them off. In addition, fine-tuning can be achieved through signals that amplify or downmodulate responses. The complexity in signal transduction pathways that regulate these responses is daunting. Even terminal responses, such as degranulation by effector cells in the immune system, do not follow a

hankering

擦掉

incarcerate

朝圣者

Anti-Leishmania Effector Functions of CD4, Th1 Cells and Early Events Instructing Th2 Cell Developmemmalian host. In contrast, mice from BALB strains are unable to control infection and develop progressive disease. Resistance and susceptibility have been correlated with the appearance of parasite-specific Th1 or Th2 cells, respectively(1). Furthermore, the passive transfer of .-specific Th1 or Th2

Feedback

Genetic Control of the T Cell Response to , Infectionby CD4. Th1 cells (1,2). Th1 cells secrete the potent macrophage activator IFN-γ, thus stimulating effective killing of this parasite (1,3). A few inbred mouse strains, such as BALB/c and SWR, fail to control parasite replication. This failure results in progressive lesion development, spread to vis

mitral-valve

plasma