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1 to the evaluation of patients with suspected autoinflammation.
2 n and concurrent, often self-resolving, mild autoinflammation.
3 f bacteria or cancer cells, or by modulating autoinflammation.
4 ifest as immune deficiency, autoimmunity, or autoinflammation.
5 hanisms, resulting in self-tissue damage and autoinflammation.
6 nd molecular mechanisms triggering this bone autoinflammation.
7 s with more common forms of autoimmunity and autoinflammation.
8 and p.*192Cext*24 causing anakinra-sensitive autoinflammation.
9 ion of innate immunity is essential to avoid autoinflammation.
10 with features of neutrophil-mediated sterile autoinflammation.
11 hologies as diverse as fibrosis, cancer, and autoinflammation.
12 RNAs, may play a role in the pathogenesis of autoinflammation.
13 ral infection but can also drive detrimental autoinflammation.
14 al lymphoproliferation, lymphomagenesis, and autoinflammation.
15 of the inflammatory nexus and how to prevent autoinflammation.
16 nfection, and mechanisms of autoimmunity and autoinflammation.
17        These data suggest a role for SFKs in autoinflammation.
18 lify immune responses, eventually leading to autoinflammation.
19 te clinical and transcriptomic resolution of autoinflammation.
20 mimicking monogenic inborn errors underlying autoinflammation.
21 al-induced cell death, IL-1beta release, and autoinflammation.
22 e context of bacterial infection or fibrotic autoinflammation.
23 kes a balance between antiviral immunity and autoinflammation.
24 tes to autoreactive CD4 T cell-mediated skin autoinflammation.
25 levels of serum cytokines typifying profound autoinflammation.
26 inase domain mutation (D849V) develop lethal autoinflammation.
27 activation of the inflammasome, and in human autoinflammation.
28 th variable symptoms of immunodeficiency and autoinflammation.
29 cleic acids as non-self and the induction of autoinflammation.
30 cating that interferons are not required for autoinflammation.
31 dictive signatures in human autoimmunity and autoinflammation.
32 fest with immunodeficiency, autoimmunity, or autoinflammation.
33 hogenic signatures in human autoimmunity and autoinflammation.
34 eventing development of immunodeficiency and autoinflammation.
35 efense against infections, autoimmunity, and autoinflammation.
36 ultaneously suffer from immunodeficiency and autoinflammation.
37 a and prevention of IFN-alpha/beta-dependent autoinflammation.
38 c fever, and fatal or near-fatal episodes of autoinflammation.
39 uently Th17 cell-dominant immunopathology in autoinflammation.
40 f the type I interferon response can lead to autoinflammation.
41 port, supporting a role for mediator-induced autoinflammation.
42  Th17 cells is related to the development of autoinflammation.
43 n dsRNA and prevents recognition by MDA5 and autoinflammation.
44 id not fully prevent APLAID mutant mice from autoinflammation.
45 infancy owing to uncontrolled IFN-I-mediated autoinflammation.
46 crocephaly, liver dysfunction, and recurrent autoinflammation.
47 use cold urticaria, antibody deficiency, and autoinflammation.
48 cts in components of inflammasomes can cause autoinflammation.
49 ced immune responses and prevent detrimental autoinflammation(11-16).
50 isk features (ie, intractable infections and autoinflammation), 25 (45%) were adolescents and young a
51 y (23.1%), opportunistic infections (15.7%), autoinflammation (29.6%), and malignancy (16.8%) identif
52 ar to those found in patients with AGS cause autoinflammation(7-12).
53 he first HSCT was associated with relapse of autoinflammation, a second HSCT was performed.
54 me instability in a mouse model of monogenic autoinflammation, after exogenous DNA damage and spontan
55 rent and/or severe infections, autoimmunity, autoinflammation, allergies, and cancer.
56 e susceptibility to infection, autoimmunity, autoinflammation, allergy and/or malignancy(1).
57 mmune dysregulation, including autoimmunity, autoinflammation, allergy, and malignancy predisposition
58 al molecular strategies acquired to regulate autoinflammation and antiviral responses.
59 disease mechanisms that initiate and sustain autoinflammation and autoimmunity and that are caused by
60  understanding of the pathogenic pathways of autoinflammation and autoimmunity in RMDs, as well as th
61 ophage and T-cell populations in the airway, autoinflammation and autoimmunity, aberrant fibrosis, ac
62 ndolysosome-resident transporter linked with autoinflammation and autoimmunity.
63 nrelated families with a similar syndrome of autoinflammation and autoimmunity.
64 ing disease-directed therapies aim to dampen autoinflammation and block cellular responses to IFN pro
65 encies present with severe immunodeficiency, autoinflammation and glycogen storage disease.
66 sms by which UBA1 mutations cause multiorgan autoinflammation and haematological disease are unclear.
67 Stat1(-/-)Pdgfrb(+/D849V) ) are rescued from autoinflammation and have improved life span compared wi
68 w that keratinocytes play a key role in skin autoinflammation and identify autophagy modulation of IL
69 riggers that induce inflammation, we propose autoinflammation and immunodeficiency as continuous clin
70 s, consistent with the unique association of autoinflammation and immunodeficiency in these patients.
71 /HOIL1 in humans and Sharpin in mice lead to autoinflammation and immunodeficiency, but the mechanism
72 lated male patients with early onset mucosal autoinflammation and inflammatory bowel disease (IBD) ch
73 tance of the ER-Golgi axis in the control of autoinflammation and inform therapeutic strategies in CO
74       We report three Moroccan siblings with autoinflammation and mycobacterial disease who are homoz
75 d with a fatal syndrome consisting of severe autoinflammation and progredient leukoencephalopathy wit
76                               Myeloid-driven autoinflammation and progressive bone marrow failure lea
77 ) and characterized by heterogenous systemic autoinflammation and progressive hematologic manifestati
78 ndividuals with DS, which contribute to both autoinflammation and severe infections.
79 of the control of repetitive element-induced autoinflammation and suggests that patients with hnRNPC-
80        This Review presents the evidence for autoinflammation and the evidence for autoimmunity in AS
81 roduce TH17 cell subsets as novel players in autoinflammation and thus novel therapeutic targets in a
82  blockade is the treatment of choice for the autoinflammation and vascular manifestations.
83 mutations in CECR1 DADA2 results in variable autoinflammation and vasculopathy (recurrent fevers, liv
84  for immune surveillance, protection against autoinflammation, and appropriate responses to allergens
85 ich includes immunodeficiency, autoimmunity, autoinflammation, and cancer.
86 ith far-reaching roles in antiviral defense, autoinflammation, and cancer.
87 r cGAS influences the outcome of infections, autoinflammation, and cancer.
88 s and manifests with both myelodysplasia and autoinflammation, and could give insight into this biolo
89  circuitry that regulate tissue homeostasis, autoinflammation, and host defense.
90 ation leads to atopic disease, autoimmunity, autoinflammation, and increased infection.
91 86C change causing neonatal-onset cytopenia, autoinflammation, and recurrent hemophagocytic lymphohis
92 nfection often associated with autoimmunity, autoinflammation, and/or malignancy.
93                                              Autoinflammation as a distinct disease category was firs
94       These findings implicate IL-1-mediated autoinflammation as contributing to the development and
95 ysregulation with monogenic autoimmunity and autoinflammation, as well as recently described IEI with
96                             We show that the autoinflammation-associated H443P mutant is altered in i
97 ot experiencing clinically overt episodes of autoinflammation at the time of sampling.
98            We also explore the overlap among autoinflammation, autoimmunity and immunodeficiency, and
99 e immune system that cause immunodeficiency, autoinflammation, autoimmunity, allergy and/or cancer.
100 l as immune dysregulatory conditions such as autoinflammation, autoimmunity, and allergy.
101 entation involving both immunodeficiency and autoinflammation/autoimmunity.
102 tation in DPP9 leads to severe infancy-onset autoinflammation because of unleashed inflammasome activ
103 ur patients suffer from chronic and systemic autoinflammation, but not severe viral infections.
104 the type I interferonopathies indicates that autoinflammation can be both interferon and noninterfero
105  (ii) autoantigenic stimulation with sterile autoinflammation can lead to tolerance.
106 sorders, including rare genetic syndromes of autoinflammation, cardiovascular diseases, neurodegenera
107 ey component in TLR trafficking, can lead to autoinflammation caused by increased TLR activity.
108 erential diagnosis of males with adult-onset autoinflammation characterized by systemic symptoms and
109                    A patient with multiorgan autoinflammation, combined immunodeficiency, subclinical
110 e spectrum of periodic fever syndromes (PFS)/autoinflammation diseases is continuously expanding.
111              We report an infant who died of autoinflammation due to a homozygous missense mutation (
112 R are the primary in vivo effectors of fatal autoinflammation following the loss of ADAR1p150.
113 a from a cohort of undiagnosed patients with autoinflammation from academic hospitals in The Netherla
114 time, our understanding of the mechanisms of autoinflammation has expanded beyond IL-1 to additional
115  with neonatal-onset pancytopenia and severe autoinflammation/hemophagocytic lymphohistiocytosis requ
116 mmunological disease continuum that includes autoinflammation, immunodeficiency, autoimmunity and ato
117 seemingly contradictory clinical phenotypes: autoinflammation, immunodeficiency, or both.
118    We sought to study the molecular basis of autoinflammation in a patient with severe infancy-onset
119 g steady state but becomes functional during autoinflammation in antagonizing mucosal damage.
120 e pathologies including immunodeficiency and autoinflammation in both humans and mice, but microbial
121 ate the mechanisms regulating NLRP3-mediated autoinflammation in human disease, characterizing the ro
122                  The mechanisms that mediate autoinflammation in mevalonate kinase deficiency, a peri
123 th in vitro findings, IL-1beta induction and autoinflammation in MSU crystal-induced peritonitis was
124 ffective option to cure cytopenia and severe autoinflammation in PAMI syndrome and may be a curative
125 raction between CARD8 and NLRP3 can regulate autoinflammation in patients.
126 ems, and activating mutations in NLRC4 cause autoinflammation in patients.
127 tic approach to investigate the mechanism of autoinflammation in Pdgfrb(+/D849V) mice and test the hy
128  overlap in the features of autoimmunity and autoinflammation in RMDs.
129 me (CAPS) patients with NLRP3 mutations have autoinflammation in skin, joints, and eyes, but not in t
130 ath pathways that has solidified the role of autoinflammation in the pathogenesis of human disease.
131 ermin D-dependent pathway and directly drive autoinflammation in vivo.
132                   This distinguishes it from autoinflammation in which the innate immune system is dy
133  CAPS phenotype with many characteristics of autoinflammation, including amyloidosis.
134 on chain assembly complex (LUBAC), underlies autoinflammation, infections, and amylopectinosis.
135          Remarkably, RdRP mice never develop autoinflammation, interferonopathy, or other discernible
136  inherited disorder characterized by chronic autoinflammation, invasive bacterial infections and musc
137 ns in humans cause lethal fulminant systemic autoinflammation (IPEX syndrome).
138                                              Autoinflammation is a sterile inflammatory process resul
139 is issue of JEM, Baldo et al. show that this autoinflammation is driven by a vicious cycle through ne
140                                              Autoinflammation is driven by TNF-induced RCD as patient
141              Yet, how IL-10 prevents mucosal autoinflammation is incompletely understood.
142        With these developments, the field of autoinflammation is moving from a gene-centric view of i
143 ity of the disease, while the development of autoinflammation is not affected by deficiencies in Toll
144 nk between neutrophils and a self-sustaining autoinflammation loop in pustular psoriasis.
145  increased risk of infections, autoimmunity, autoinflammation, malignancy, and allergic disorders.
146              In this study, we show that the autoinflammation observed in Mefv(V726A/V726A) mice is m
147 OF) variants can develop myeloid malignancy, autoinflammation, or both, if some or all of their leuko
148 h cells are known to be enriched at sites of autoinflammation, our finding that they are highly proin
149 utrophil-derived IL-26 drives the pathogenic autoinflammation process by inducing the expression of I
150 bute to understand the role of miR-197-3p in autoinflammation process.
151 natal-onset cytopenia with dyshematopoiesis, autoinflammation, rash, and HLH.
152 the impaired retrograde transport results in autoinflammation remains poorly understood.
153  and age of onset of cytopenia and extent of autoinflammation representing major differences.
154 e the age-dependent lymphoid hypertrophy and autoinflammation seen in animals with a complete knockou
155 ter consisting of humoral immune deficiency, autoinflammation, susceptibility to herpesvirus infectio
156 on of actin polymerization leads to systemic autoinflammation that is reduced when IL-18 is deleted b
157 pathophysiological concepts of IL-1-mediated autoinflammation, the epidemiological and clinical featu
158 ver 20 years ago, it was first proposed that autoinflammation underpins a handful of rare monogenic d
159 -like cells in the cochlea can mediate local autoinflammation via activation of the NLRP3 inflammasom
160                               In this model, autoinflammation was caused by mutation in the actin reg
161 g of the spectrum of organ manifestations in autoinflammation was expanded by the discovery of two no
162                               The concept of autoinflammation was introduced to this field, and medic
163              Susceptibility to infection and autoinflammation were common with both GOF and LOF varia
164 ent hepatic, neuronal necroptosis, and overt autoinflammation were not detected.
165                             Pyrin-associated autoinflammation with neutrophilic dermatosis (PAAND) is
166 diterranean fever (FMF) and Pyrin-associated autoinflammation with neutrophilic dermatosis (PAAND).
167        Missense mutations in PLCG2 can cause autoinflammation with phospholipase C gamma 2-associated
168 onset (mean age 67 years, range 47-79 years) autoinflammation with systemic symptoms, elevated inflam

 
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