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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 irculating immune cell numbers or neutrophil degranulation responses.
5 dissociable aggregates to stimulate Ca2+ and degranulation responses.
6 strong heterogeneity of individual mast cell 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  rise to NK cells that exhibit an attenuated degranulation response but robustly produce inflammatory
10 esults in modest defects in phagocytosis and degranulation responses but a profound block in superoxi
11 is kinase was required for integrin-mediated degranulation responses, but was not involved in adhesio
12 ation of cytokine gene transcription and the degranulation response by modulating JNK activity in BMM
13 ism, dependent on FcgammaR-mediated enhanced degranulation responses by MCs.
14 releasing factor (CRF) system potentiates MC degranulation responses during IgE-mediated anaphylaxis
15                        In contrast, Ca2+ and degranulation responses elicited by effectively irrevers
16 ogether, these findings suggest that reduced degranulation responses in desensitized MCs arise from a
17 therwise unstimulated Eo, produced prominent degranulation responses in Eo primed by granulocyte-macr
18 ptor-mediated Ca(2+) influx stimulate strong degranulation responses in these variant cells.
19 vitro revealed that whereas they have normal degranulation responses, they secrete elevated levels of
20 ing: 1) term pregnancy dNK have an increased degranulation response to K562 and PMA/ionomycin but low
21 terized by increased neutrophil adhesion and degranulation responses to LTB4.
22   These cyclic dimers do not trigger Ca2+ or degranulation responses under a variety of conditions.
23  stimulation, demonstrating that the NK cell degranulation response was also primed.
24 n response was significantly reduced and CD8 degranulation response was even more enhanced (P<0.05).
25 necrosis factor-alpha-activated TECs, the NK degranulation response was significantly reduced and CD8
26                By comparison, robust NK cell degranulation responses were observed both before and af
27 nsible for triggering essentially all of the degranulation response, whereas aggregates with poorly d
28 mically distinct ENMs caused a range of mast degranulation responses, with smaller sized Ag NPs (5 nm