ライフサイエンスコーパス: alarmin

1 hypothesized that GNLY might function as an alarmin.

2 duction of Th2 responses and functions as an alarmin.

3 ells that were drawn to injured cartilage by alarmins.

4 sidered as endogenous multifunctional immune alarmins.

5 ion of CVB3 led to a downregulation of these alarmins.

6 lled damage associated molecular patterns or alarmins.

7 erminal centers, and increased expression of alarmins.

8 ersely, a lack of biologically active S100A8 alarmin, achieved by antibody neutralization or by using

9 and immune responses through production of "alarmins." Alarmins are endogenous molecules secreted fr

10 g liver injury; however, a link between this alarmin and ALD has not been established.

11 oup nucleosome-binding protein 1) as a novel alarmin and demonstrate that it contributes to the induc

12 In particular, GRHL3 suppressed a number of alarmin and other proinflammatory genes after immune inj

13 o-inflammatory cytokines IL-1beta and IL-18, alarmins and endogenous danger-associated molecular patt

14 Thus, alarmins and founder gene mutations in MDSs license a co

15 rden, PMN infiltration, the presence of S100 alarmins and inflammatory cytokines and chemokines.

16 Liver-derived HRG, similar to alarmins, appears to be an endogenous molecular factor p

17 Alarmins are a group of structurally diverse host defens

18 Alarmins are endogenous mediators capable of promoting t

19 Alarmins are endogenous mediators that can induce recrui

20 responses through production of "alarmins." Alarmins are endogenous molecules secreted from cells un

21 Alarmins are endogenous molecules that are constitutivel

22 derived PAMPs and that endogenously produced alarmins are not sufficient.

23 ion and tissue damage, virulence factors and alarmins are pro-inflammatory and induce activation of v

24 or lipoteichoic acid as would be expected if alarmins are sufficient to activate the TLRs.

25 oxin-free" particles as would be expected if alarmins are sufficient to activate the TLRs.

26 ction of lipid mediators of inflammation and alarmins, are just some examples of how advances in immu

27 emodelling signature and identify endogenous alarmins as amplifiers of the inflammatory response that

28 ly cleaved IL-18 and IL-33, two IL-1-related alarmins, as well as the cytokine IL-15, which is import

29 the presence of microbial danger signals or alarmins associated with cytopathic damage.

30 urine epidermis, IL-33 behaved similar to an alarmin, being constitutively expressed in keratinocyte

31 ad trauma, released galectin-3 may act as an alarmin, binding, among other proteins, to TLR-4 and pro

32 Cleavage of the alarmins by HC and hCG suggests a function in regulating

33 e-associated molecular pattern molecules (or alarmins) by engaging the receptor for advanced glycatio

34 nger hypothesis," it was recently shown that alarmins can also directly sense and report damage by si

35 Y is the first identified lymphocyte-derived alarmin capable of promoting APC recruitment, activation

36 s that uncontrolled and excessive release of alarmins contributes to the dysregulated processes seen

37 Thus, extracellular HMGN1 acts as a novel alarmin critical for LPS-induced development of innate a

38 Interleukin-33 (IL-33) is an alarmin cytokine from the IL-1 family.

39 l expression of IL-33, an epithelium-derived alarmin cytokine, in patients with EoE.

40 state and after in vivo stimulation with the alarmin cytokines IL-25 and IL-33.

41 Innate cells respond to 'alarmin' cytokines (IL-25, IL-33, TSLP) by producing IL-

42 utrophils, T cells, reactive oxygen species, alarmins, danger-associated molecular patterns, purinerg

43 recently been attributed to the epithelial "alarmin" defense system.

44 ting a potential pathophysiological role for alarmin/DNA complexes in contributing to inflammation.

45 is a nuclear protein and may function as an "alarmin" during cell death, a process that is uncommon i

46 ng history; complement products function as "alarmins" during innate responses.

47 We conclude that IL-1alpha acts as an alarmin essential for leukocyte recruitment and protecti

48 The alarmin family has been expanding in terms of both numbe

49 established in host immune responses, termed alarmins, has been largely overlooked in cancer biology.

50 Conversely, alarmins have also been found to play a major role in th

51 r-associated molecular pattern molecules, or alarmins, have been recognized as signaling mediators of

52 The alarmin high mobility group box 1 (HMGB1) can be release

53 Here, we investigated whether the alarmin high mobility group box 1 (HMGB1) mediates age-a

54 The alarmin high mobility group box 1 (HMGB1) was released b

55 omers, but not monomers and fibrils, and the alarmin high-mobility group box-1 protein (HMGB-1) could

56 D8(+) Treg cell-surface Tim-3 binding to the alarmin, high-mobility group box 1 (HMGB-1).

57 Here, we provide an update and overview on alarmins, highlighting the areas that may benefit from t

58 LR-5 signalling mediates upregulation of the alarmin HMGB1 (High Mobility Group Box 1) in wound-induc

59 We demonstrate that HS/R through the alarmin HMGB1 induces IL-23 secretion from macrophages i

60 The secreted alarmin HMGB1 is a proinflammatory partner, inducer, and

61 erate effector CD8(+) T cells by binding the alarmin HMGB1 via CD24 and presenting it to RAGE(+) T ce

62 formation, and elevated concentration of the alarmins HMGB1 and histone 3 in the lungs.

63 icle, we present a novel role for two potent alarmins, human beta-defensin 2 and 3 (HBD2 and 3), in p

64 s passed since the conceptualization of the "alarmin" hypothesis.

65 se, but not MC tryptase, also degraded other alarmins, i.e. biglycan, HMGB1, and IL-33, a degradation

66 es the release of mature IL-1beta and of the alarmin IL-1alpha Dying cells release IL-1alpha also, in

67 ression by B cells is induced by the mucosal alarmin IL-33 (ref.

68 The alarmin IL-33 plays a role in a wide range of pathologie

69 ) show that injured spinal cord releases the alarmin IL-33 to drive chemokines that recruit monocytes

70 n response to inflammatory mediator IL-18 or alarmin IL-33, but not by TCR signaling that is required

71 shortly after infection, upregulation of the alarmin IL-33, which drives type 2 immunity, and activat

72 in the context of diseases triggered by the alarmin IL-33.

73 ression by B cells is induced by the mucosal alarmin IL-33.

74 ice was dependent on TSLP, but not the other alarmins IL-25 and IL-33.

75 Here, we provide evidence that the "alarmin" IL-33, a nuclear cytokine that activates type 2

76 en together, we report that the IL-1 family "alarmins" IL-18 and IL-33 in addition to amplifying both

77 enomewide association studies implicate the 'alarmin' IL-33 in asthma, but its role in mast cell-ASM

78 Overproduction of the UA alarmin in the local microenvironment plays a critical r

79 on exhibited elevated levels of vaginal S100 alarmins in both vaginal epithelia and secretions in the

80 -products (RAGE) revealed the involvement of alarmins in inflammatory gene expression, which was foun

81 matory condition of VVC is initiated by S100 alarmins in response to C. albicans, which stimulate pol

82 ovide a general view on the participation of alarmins in the induction of innate and adaptive immune

83 ities by grouping them under the novel term 'alarmins', in recognition of their role in mobilizing th

84 functions as an endogenous danger signal, or alarmin, in response to tissue damage.

85 AGEs and other alarmins inadvertently prime innate signaling through mu

86 The function of several alarmins-including the defensins, LL-37, and HMGB1-in tu

87 In CVB3-infected RAW macrophages, both alarmins increased MIP-2 (macrophage inflammatory protei

88 ponse in mucosal candidiasis as well as S100 alarmin induction, this study aimed to determine whether

89 r in vivo in the presence or absence of S100 alarmins initiated by several approaches.

90 mediary of the citric acid cycle, acts as an alarmin, initiating and propagating danger signals resul

91 icroglia at sites of SCI rapidly express the alarmin interleukin (IL)-1alpha, and that infiltrating n

92 nts, the respiratory epithelium releases the alarmin interleukin (IL)-33 to elicit a rapid immune res

93 sis are selectively targeted by the cytokine/alarmin interleukin (IL)-33.

94 ular mechanisms that drive expression of the alarmin interleukin-33 (IL-33) in endothelial cells are

95 the recipient microbiome, the impact of the alarmin interleukin-33 on alloreactivity, and the role o

96 Here we identify the nuclear alarmin, interleukin (IL)-33, as an important regulator

97 le of ILC2 in translating epithelial-derived alarmins into downstream adaptive type-2 responses via d

98 These results suggest that S100A8 alarmin is sufficient, but not necessary, to induce PMN

99 kedly increased epithelial expression of the alarmin-like cytokine IL-33 in nasal polyps, as compared

100 er-1 prevented the upregulation of IL-33, an alarmin linked to necroptosis, and other chemokines and

101 pecific degradation of virulence factors and alarmins may depend on the presence of accessible extend

102 er the Th17 pathway plays a role in the S100 alarmin-mediated acute inflammation during VVC using the

103 h-mobility group box 1 (HMGB1), a prototypic alarmin, mediates the systemic inflammatory response syn

104 also with C3a, CpG DNA oligonucleotides, and alarmin molecules such as HMGB1 to initiate a proinflamm

105 The alarmins myeloid-related protein (MRP)8 and MRP14 are th

106 ge-associated molecular patterns, so-called "alarmins," orchestrates the immune response.

107 It has recently become clear that alarmins play important roles as initiators and particip

108 is mediated by chemotactic S100A8 and S100A9 alarmins produced by vaginal epithelial cells in respons

109 such activation is important for release of alarmins, pyroptosis, and early IFN-gamma production by

110 his stress response was triggered in part by alarmin recognition and was blunted in CD24 sensor- and

111 immunostimulatory bactericidal proteins and alarmins, relative to lupus and control neutrophils.

112 Here, we identified H. polygyrus Alarmin Release Inhibitor (HpARI), an IL-33-suppressive

113 n damaged areas where they degraded IL33, an alarmin released by epithelial cells during tissue damag

114 We hypothesized that IL33, an alarmin released early after tissue injury and a known r

115 Taken together, these studies indicate that alarmins represent potential new targets for manipulatio

116 These data suggest that the vaginal S100 alarmin response to Candida does not require the cells o

117 as C-reactive protein, myeloperoxidase, and alarmin S100-A9.

118 o data and determine the requirement for the alarmin S100A8 in the PMN response and to evaluate patte

119 The alarmin S100A8/A9 has been implicated in the induction o

120 In conclusion, the alarmin S100A8/S100A9 is a valuable and sensitive molecu

121 l molecular imaging, we demonstrate that the alarmin S100A8/S100A9 serves as a sensitive local and sy

122 The alarmins S100A8 and S100A9 are damage-associated molecul

123 hanistically, pyroptosis is triggered by the alarmin S100A9 that is found in excess in MDS HSPCs and

124 y function as an endogenous danger signal or alarmin, similar to IL-1alpha or high-mobility group box

125 tly were found to be activated by endogenous alarmins such as fragmented extracellular matrix protein

126 mage-associated molecular patterns including alarmins such as HMGB1 and IL-1beta, Toll-like receptors

127 n this article, we review the involvement of alarmins such as IL-1alpha, IL-33, IL-16, and high-mobil

128 ng the target and source of adipocytokines, 'alarmins' such as interleukin-9 (IL-9) and interleukin-3

129 Alarmins, such as ATP, likely play a pivotal role in the

130 y associated with the presence of endogenous alarmins, such as extracellular ATP (an indicator of cyt

131 c proteins, cytokines, chemokines, or immune alarmins, such as granulysin (GNLY), leading to the exte

132 EDN to have the properties of an endogenous alarmin that alerts the adaptive immune system for prefe

133 High molecular group S (HMGB1) is a major alarmin that binds to the receptor for advanced glycatio

134 servations suggest that IL-36gamma may be an alarmin that signals the cause, e.g., viral infection, o

135 The damaged epithelium is a source of alarmins that activate the innate immune system, yet the

136 d persistent overexpression of extracellular alarmins that can trigger inflammation via pattern recog

137 ibility that IL-33 may function as a nuclear alarmin to alert the innate immune system after injury o

138 mune cells secrete HMGB1 as an extracellular Alarmin to signal tissue damage.

139 However, the relevance of alarmins to the induction of adaptive immune responses r

140 unclear, although IL-33 might function as an alarmin triggered by damage-associated molecular pattern

141 terleukin-1alpha and interleukin-33 exhibit 'alarmin'-type properties that can signal tissue or cell

142 and, is an IL-1 family member and acts as an alarmin, we explored the ST2 pathway in human and mouse

143 Two epithelial alarmins were measured longitudinally in bronchoalveolar

144 Alarmins, which are locally released during cellular str