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- 저자 : Yoshiko Emoto (검색결과 2 건)
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Masashi Emoto,Masakazu Kaneko,Yoshiko Emoto 연세대학교의과대학 2016 Yonsei medical journal Vol.57 No.2
Macrophages (Mo|) play a pivotal role in the protection system by recognizing and eliminating invading pathogenic bacteria. Phagocytosis and the killing of invading bacteria are major effector functions of Mo|. Although the phagocytic and bactericidal activitiesof Mo| have been analyzed via several methods using a light microscope, a fluorescence microscope, or a fluorescence-activatedcell sorter, expensive materials and equipment are usually required, and the methods are rather complicated. Moreover, it is impossible to determine both the phagocytic and bactericidal activities of Mo| simultaneously using these methods. In this review,we describe a simple, reproducible, inexpensive, yet old-fashioned method (antibiotic protection assay) for determining the phagocytic and bactericidal activities of Mø.
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Intracellular Bacterial Infection and Invariant NKT Cells
Masashi Emoto,Yoshiko Emoto 연세대학교의과대학 2009 Yonsei medical journal Vol.50 No.1
The invariant (i) natural killer (NK)T cells represent a unique subset of T lymphocytes which express the Valpha14 chain of the T cell receptor (TCR), that recognizes glycolipid antigens presented by the nonpolymorphic major histocompatibility complex (MHC) class I-like antigen presentation molecule CD1d, and they participate in protection against some microbial pathogens. Although iNKT cells have originally been regarded as T cells co-expressing NKR-P1B/C (NK1.1: CD 161), they do not seem to consistently express this marker, since NK1.1 surface expression on iNKT cells undergoes dramatic changes following facultative intracellular bacterial infection, which is correlated with functional changes of this cell population. Accumulating evidence suggests that NK1.1 allows recognition of "missing-self", thus controling activation/inhibition of NK1.1-expressing cells. Therefore, it is tempting to suggest that iNKT cells participate in the regulation of host immune responses during facultative intracellular bacterial infection by controlling NK1.1 surface expression. These findings shed light not only on the unique role of iNKT cells in microbial infection, but also provide evidence for new aspects of the NK1.1 as a regulatory molecule on these cells.
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