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1 receptor aggregation at equilibrium and the degranulation response.
2 estin but not internalization terminates the degranulation response.
3 ne C4 or superoxide anion nor any detectable degranulation response.
4 strong heterogeneity of individual mast cell degranulation responses.
5 dissociable aggregates to stimulate Ca2+ and degranulation responses.
6 irculating immune cell numbers or neutrophil degranulation responses.
7 ged in vitro NK cell cytokine production and degranulation responses after restimulation of PBMCs wit
8 is, cell adhesion, free radical release, and degranulation, responses associated with infection and i
9 esults in modest defects in phagocytosis and degranulation responses but a profound block in superoxi
10 is kinase was required for integrin-mediated degranulation responses, but was not involved in adhesio
11 ation of cytokine gene transcription and the degranulation response by modulating JNK activity in BMM
14 ogether, these findings suggest that reduced degranulation responses in desensitized MCs arise from a
15 therwise unstimulated Eo, produced prominent degranulation responses in Eo primed by granulocyte-macr
17 vitro revealed that whereas they have normal degranulation responses, they secrete elevated levels of
19 These cyclic dimers do not trigger Ca2+ or degranulation responses under a variety of conditions.
21 n response was significantly reduced and CD8 degranulation response was even more enhanced (P<0.05).
22 necrosis factor-alpha-activated TECs, the NK degranulation response was significantly reduced and CD8
24 nsible for triggering essentially all of the degranulation response, whereas aggregates with poorly d
25 mically distinct ENMs caused a range of mast degranulation responses, with smaller sized Ag NPs (5 nm
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