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Recognition of Listeria monocytogenes infection by natural killer cells: Towards a complete picture by experimental studies in rats

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INNATE IMMUNITY
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SAGE PUBLICATIONS LTD
DOI: 10.1177/17534259231178223

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NK cells; rat NK-subsets; MHC-I; Clr ligands; NKR-P1 receptors; Ly49 receptors; Listeria monocytogenes; rats

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The study focuses on the cellular immune responses in animal disease models, particularly the role of natural killer (NK) cells in the host-pathogen interaction with Listeria monocytogenes (LM) bacterium. The research reveals that NK cell ligands, including MHC class I molecules and Clr molecules, are influenced in LM-infected cells, leading to the stimulation of rat NK cells. These findings contribute to our understanding of how NK cells recognize and respond to LM infection.
The study of cellular immune responses in animal disease models demands detailed knowledge of development, function, and regulation of immune cells, including natural killer (NK) cells. Listeria monocytogenes (LM) bacterium has been explored in a large area of research fields, including the host pathogen interaction. Although the importance role of NK cells in controlling the first phase of LM burden has been investigated, the interaction between NK cells and infected cells in details are far from being comprehended. From in vivo and in vitro experiments, we can drive several important pieces of knowledge that hopefully contribute to illuminating the intercommunication between LM-infected cells and NK cells. Experimental studies performed in rats revealed that certain NK cell ligands are influenced in LM-infected cells. These ligands include both classical- and non-classical MHC class I molecules and C-type lectin related (Clr) molecules that are ligands for Ly49- and NKR-P1 receptors respectively. Interaction between these receptors:ligands during LM infection, demonstrated stimulation of rat NK cells. Hence, these studies provided additional knowledge to the mechanisms NK cells utilise to recognise and respond to LM infection outlined in the current review.

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