ライフサイエンスコーパス: cytokine storm

1 ponse leading to a potentially catastrophic "cytokine storm".

2 ng systemic inflammatory response, termed a 'Cytokine Storm'.

3 ift hyperinflammatory response typified by a cytokine storm.

4 othelial barrier disruption and uncontrolled cytokine storm.

5 nsplantation to avoid the adverse effects of cytokine storm.

6 hat resulted in an elevated pro-inflammatory cytokine storm.

7 y mediators implicated in the TSS-associated cytokine storm.

8 tivation in BALB/c mice was accompanied by a cytokine storm.

9 (high) monocytes and neutrophils and fuels a cytokine storm.

10 ce resulted in induction of rapid and lethal cytokine storm.

11 tory syndromes characterized by uncontrolled cytokine storm.

12 n thought to drive excessive inflammation in cytokine storm.

13 icity involve strain selection and a massive cytokine storm.

14 event where virus-specific T cells induce a cytokine storm.

15 participants who all developed a devastating cytokine storm.

16 g, indicating a common pathway inhibition of cytokine storm.

17 stemic uncontrolled inflammatory response or cytokine storm.

18 mechanisms that are important in initiating cytokine storm.

19 tics for infectious disease characterized by cytokine storm.

20 g endothelial cells as central regulators of cytokine storm.

21 anced vascular permeability, likely due to a cytokine storm.

22 entify new proteins involved in triggering a cytokine storm.

23 e them to be eliminated by a proinflammatory cytokine storm.

24 overly exuberant immune response, termed a "cytokine storm," accompanies virus-induced acute respira

25 A cytokine storm also occurred, with GVHD-specific secreti

26 Whether human cytokine storm also plays a similar role is not clear.

27 anti-CD28 antibody TGN1412 caused a massive cytokine storm and multiorgan failure in six healthy hum

28 ines with neutralizing antibodies blunts the cytokine storm and protects the host.

29 combination therapy induces an intratumoral "cytokine storm" and extensive lymphocyte infiltration.

30 injury (ALI) characterized by vascular leak, cytokine storm, and infiltration of mononuclear cells in

31 ivity impairs bacterial clearance, elicits a cytokine storm, and precipitates septic shock.

32 suggest that strain selection and a massive cytokine storm are major factors behind increased pathog

33 Although the cytokine storm associated with GVHD leads to expression

34 a, pneumonia, and septicemia and averted the cytokine storm associated with septic infection but had

35 y that is independent of NF-kappaB triggered cytokine storm but dependent on cellular egress.

36 agonist significantly inhibited PVM-elicited cytokine storm by blunting the PVM-specific CD8(+) T cel

37 pattern recognition receptors initiating the cytokine storm by extensive cross-talk.

38 ells infiltrated into the lung, initiating a cytokine storm by their production of gamma interferon (

39 -A4, Sema3A (semaphorin 3A), exacerbates the cytokine storm caused by TLR agonists and bacterial seps

40 cute inflammatory phase of GVHD, attenuating cytokine storm, CD8+ T-cell proliferation/activation, an

41 D4(+)T cell compartment, high viremia, and a cytokine storm characterize the early days after HIV inf

42 These pathogenic T cells initiated a cytokine storm characterized by high levels of tumor nec

43 ogressors (RDPs) had earlier and more robust cytokine storms, compared with slow disease progressors

44 ar, induction of high levels of interferon ("cytokine storms"), coupled with evasion of its effects,

45 is believed to contribute to the pathogenic cytokine storm described in severe dengue patients, but

46 marrow transplantation where an inflammatory cytokine storm dominates.

47 ctively), suggesting the faster and stronger cytokine storm during AHI could promote disease progress

48 The cytokine storm during influenza virus infection, whereby

49 Cytokine storm during viral infection is a prospective p

50 virus infection, robust cytokine production (cytokine storm), excessive inflammatory infiltrates, and

51 ncluding IL-6 and IFN-gamma, contribute to a cytokine storm formerly known as "toxemia." A more preci

52 ecific CD4 T cells and was associated with a cytokine storm, generalized inflammation, and multi-orga

53 Cytokine storm has been postulated as one of the major c

54 el genetic and immunotherapeutic triggers of cytokine storm have been identified.

55 ressed secretion of HMGB1, reduced the human cytokine storm, human lymphocyte apoptosis, and rescued

56 infection of Kupffer cells and the following cytokine storm.IMPORTANCE Immunocompromised human patien

57 odulatory interventions aimed at controlling cytokine storm in AHI may be beneficial to slow eventual

58 volved in endothelial barrier disruption and cytokine storm in experimental lung injury.

59 in conjunction with alphaCD40/IL-2 prevented cytokine storms in young obese mice and protected from l

60 cytokine production in vitro and blunts the "cytokine storm" in endotoxemic mice by reducing levels o

61 on factors owing to hepatocellular necrosis, cytokine storm, increased permeability by vascular endot

62 uch as Campath) and severe (such as TGN1412) cytokine storm-inducing drugs.

63 ecan-1-null mice from the magnified systemic cytokine storm, inflammatory tissue injury, and death.

64 ests that diseases in which amplification of cytokine storm is a significant pathological component c

65 The cytokine storm is an intensified, dysregulated, tissue-i

66 Importantly, the cytokine storm is chemically treatable with specific ago

67 n contrast to influenza infection, where the cytokine storm is initiated early by the innate immune s

68 nia virus of mice (PVM), a model of RSV, the cytokine storm is initiated late in infection by the ada

69 proinflammatory cytokines, but whether this cytokine storm is the main cause of fatality or is a con

70 during H5N1 influenza virus infection, the "cytokine storm" is hypothesized to be the main cause of

71 table approach for the effective blunting of cytokine storm, leading to the improvement of clinical a

72 tion, most likely by reducing TLR4-dependent cytokine storm mediated by damage-associated molecular p

73 Thus, superantigens induce a cytokine storm not only by mediating the interaction bet

74 nt in the rats did not reproduce the massive cytokine storm observed following TGN1412 administration

75 tes to lower pathogenicity by preventing the cytokine storm observed in EBOV infection.

76 drome (SIRS) and confirm the hypothesis that cytokine storm occurs as a result of HTRs.

77 Cytokine storm of influenza virus infection is initiated

78 evere dengue has long been associated with a cytokine storm of unclear origin.

79 S) are 2 similar diseases characterized by a cytokine storm, overwhelming inflammation, multiorgan dy

80 egulates multiple ARDS GWAS genes related to cytokine storm, oxidation, and coagulation in lung micro

81 With cytokine storm playing a role in the pathogenesis of a w

82 ons uncovered the prominent direct role that cytokine storm plays in the pathogenesis, morbidity, and

83 Mouse models support the hypothesis that 'cytokine storm' plays an important role in the pathogene

84 The characteristic cytokine storm produced upon alpha-GalCer activation was

85 Current bioassays that detect cytokine storm responses in vitro rely on endothelial ce

86 t need for human tissue bioassays to predict cytokine storm responses to biologics.

87 tosis, Prf-deficient infants suffer a fatal "cytokine storm" resulting from macrophage overactivation

88 uires identification of key mediators of the cytokine storm's initial wave.

89 by dramatically increased bacterial burden, cytokine storm, striking histological abnormalities, and

90 e activation syndrome (MAS) is a devastating cytokine storm syndrome complicating many inflammatory d

91 ses increased proliferation of T cells and a cytokine storm syndrome in vivo.

92 tive conditioning regimen is hindered by the cytokine storm syndrome triggered by anti-CD3 and the hi

93 uces cytokine production and ameliorates the cytokine storm syndrome triggered by anti-CD3.

94 Cytokine storm syndromes, such as familial hemophagocyti

95 eads to the severe immune dysregulation and "cytokine storm" that is characteristic of fatal ebolavir

96 al emphasis on the principal features of the cytokine storm the mechanisms underlying this intense sy

97 This "cytokine storm" then acts on T cells in the graft, promp

98 For over two decades, we have embraced the cytokine storm theory to explain sepsis, severe sepsis a

99 The typical cytokine storm was present, with levels of interferon ga

100 fraction of T cell pools to set in motion a "cytokine storm" with severe and sometimes life-threateni

101 Central to its pathogenesis is a cytokine storm, with markedly increased levels of numero

102 hrough altered T-bet dominance to dampen the cytokine storm without impeding the generation of memory