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1 Ndfip1 deletion in Treg cells results in autoinflammatory disease.
2 uggest classification of PAPA syndrome as an autoinflammatory disease.
3 tivation by NEMO, and its absence results in autoinflammatory disease.
4 ies in patients with Schnitzler syndrome, an autoinflammatory disease.
5 host-regulated actin-dependent processes and autoinflammatory disease.
6 identify IFN-gamma as a mediator of systemic autoinflammatory disease.
7 filamentous bacteria, and an extraintestinal autoinflammatory disease.
8 ional target for therapeutic intervention in autoinflammatory disease.
9 which gain-of-function pyrin mutations cause autoinflammatory disease.
10 anean fever (FMF), the most common Mendelian autoinflammatory disease.
11 nd humans, to a propensity for infection and autoinflammatory disease.
12 hat is associated with a macrophage-mediated autoinflammatory disease.
13 aggerated and sustained responses leading to autoinflammatory disease.
14 ion induced by NALP3 mutants associated with autoinflammatory diseases.
15 entral to the pathogenesis of many monogenic autoinflammatory diseases.
16 d to the addition of gout to the spectrum of autoinflammatory diseases.
17 epidemiologically associated autoimmune and autoinflammatory diseases.
18 ons in CIAS1/cryopyrin are linked to several autoinflammatory diseases.
19 and contributes to the pathology of various autoinflammatory diseases.
20 that LDHA may be targeted therapeutically in autoinflammatory diseases.
21 at contribute to a variety of autoimmune and autoinflammatory diseases.
22 o new treatments for cytosolic DNA-triggered autoinflammatory diseases.
23 nd modulation of exaggerated inflammation in autoinflammatory diseases.
24 rapy of RA and possibly other autoimmune and autoinflammatory diseases.
25 ot in cells of patients afflicted with other autoinflammatory diseases.
26 mutations are associated with autoimmune and autoinflammatory diseases.
27 et juvenile idiopathic arthritis and related autoinflammatory diseases.
28 not in that of patients with other inherited autoinflammatory diseases.
29 tools to address infectious, autoimmune, and autoinflammatory diseases.
30 tial therapeutic target in uveitis and other autoinflammatory diseases.
31 ated genes shared by multiple autoimmune and autoinflammatory diseases.
32 to understand human systemic autoimmune and autoinflammatory diseases.
33 hology associated with several autoimmune or autoinflammatory diseases.
34 mic and local inflammatory conditions called autoinflammatory diseases.
35 receptor signaling, exhibiting a feature of autoinflammatory diseases.
36 IL-1 family because of its role in mediating autoinflammatory diseases.
37 nean fever and several of the other systemic autoinflammatory diseases, a recently recognized group o
39 ells affects inflammatory responses in human autoinflammatory disease and in mouse models of inflamma
40 iated alterations in patients with monogenic autoinflammatory disease and opens up possibilities for
42 o recognize and treat patients with systemic autoinflammatory diseases and inform our understanding o
44 genetic basis of both mendelian and complex autoinflammatory diseases, and with the recognition that
55 cell death implicated in the pathogenesis of autoinflammatory diseases as well as in disorders charac
56 me (TRAPS) is an autosomal dominant systemic autoinflammatory disease associated with heterozygous mu
57 deployment of anti-IL-1 therapies to control autoinflammatory diseases associated with aberrant infla
58 the innate immune system can cause systemic autoinflammatory diseases associated with increased IL-1
59 sum, and Acne Syndrome (PAPA syndrome) is an autoinflammatory disease caused by aberrant production o
60 culopathy with onset in infancy (SAVI) is an autoinflammatory disease caused by gain-of-function muta
62 or DIRA, to denote this autosomal recessive autoinflammatory disease caused by mutations affecting I
63 Familial Mediterranean fever (FMF) is an autoinflammatory disease caused by mutations in MEFV, wh
64 rranean fever (FMF) is an IL-1beta-dependent autoinflammatory disease caused by mutations of Mediterr
65 and perhaps treat, lupus nephritis and other autoinflammatory diseases caused by the decreased abilit
67 Polymorphisms in NOD1 are associated with autoinflammatory diseases characterized by uveitis such
68 adaptor protein PSTPIP2 are the cause of the autoinflammatory disease chronic multifocal osteomyeliti
69 ense mutations in NLRP3 result in a group of autoinflammatory diseases collectively known as the cryo
70 bryonic lethality, macrothrombocytopenia and autoinflammatory disease develop in mice carrying hypomo
71 utations in its B30.2/SPRY domain causes the autoinflammatory disease familial Mediterranean fever by
72 stinct interleukin-1beta (IL-1beta)-mediated autoinflammatory diseases: familial Mediterranean fever
73 he genes and proteins mutated in many of the autoinflammatory diseases has broadened our understandin
75 cterization of a growing number of monogenic autoinflammatory diseases has provided important insight
79 1R1, is broadly used to treat autoimmune and autoinflammatory diseases; however, blocking IL-1 increa
81 epidemiologically associated autoimmune and autoinflammatory diseases, implicating the innate immune
86 e association of mutations in NLR genes with autoinflammatory diseases indicates an important functio
88 ase-interacting protein 2 (PSTPIP2), lead to autoinflammatory disease involving extramedullary hemato
89 tor antagonist (IL-1Ra) deficiency is a rare autoinflammatory disease involving neonatal onset of pus
91 the gene encoding NLRP3 cause a spectrum of autoinflammatory diseases known as cryopyrin-associated
93 erlie familial Mediterranean fever and other autoinflammatory diseases, may predispose to vasculitis.
95 nd F-BAR protein that has been implicated in autoinflammatory disease, most notably in the PAPA syndr
96 P3/CIAS1/PYPAF1 gene are associated with the autoinflammatory diseases Muckle-Wells syndrome (MWS), f
97 mic juvenile idiopathic arthritis (sJIA), an autoinflammatory disease of unknown etiology, this appro
98 n proposed as useful therapeutics in various autoinflammatory diseases or amelioration of inflammator
103 questions that are expected to be central in autoinflammatory disease research in the coming decade.
104 ponsible for the development of a persistent autoinflammatory disease resembling chronic recurrent mu
109 flammasome defect that expands the monogenic autoinflammatory disease spectrum to include MAS and sug
110 e, and cause the autosomal dominant systemic autoinflammatory disease spectrum, termed cryopyrin-asso
111 ations in NFKB1 and suggest that a subset of autoinflammatory diseases, such as Behcet disease, can b
114 His case highlights IL-1Ra deficiency as an autoinflammatory disease that is distinct from neonatal-
115 well established genetic model of autoimmune/autoinflammatory disease that resembles systemic lupus e
116 he cause of a life-threatening but treatable autoinflammatory disease that underscores the divergent
117 matoses are a group of complex heterogeneous autoinflammatory diseases that all demonstrate excessive
118 w, we describe the genetically characterized autoinflammatory diseases, we summarize our understandin
122 ely activate these pathways underlie several autoinflammatory diseases with diverse clinical features
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