ライフサイエンスコーパス: autoinflammation

1 levels of serum cytokines typifying profound autoinflammation.

2 cleic acids as non-self and the induction of autoinflammation.

3 cating that interferons are not required for autoinflammation.

4 dictive signatures in human autoimmunity and autoinflammation.

5 fest with immunodeficiency, autoimmunity, or autoinflammation.

6 hogenic signatures in human autoimmunity and autoinflammation.

7 eventing development of immunodeficiency and autoinflammation.

8 efense against infections, autoimmunity, and autoinflammation.

9 ultaneously suffer from immunodeficiency and autoinflammation.

10 inase domain mutation (D849V) develop lethal autoinflammation.

11 a and prevention of IFN-alpha/beta-dependent autoinflammation.

12 c fever, and fatal or near-fatal episodes of autoinflammation.

13 uently Th17 cell-dominant immunopathology in autoinflammation.

14 port, supporting a role for mediator-induced autoinflammation.

15 activation of the inflammasome, and in human autoinflammation.

16 th variable symptoms of immunodeficiency and autoinflammation.

17 isk features (ie, intractable infections and autoinflammation), 25 (45%) were adolescents and young a

18 me instability in a mouse model of monogenic autoinflammation, after exogenous DNA damage and spontan

19 disease mechanisms that initiate and sustain autoinflammation and autoimmunity and that are caused by

20 ophage and T-cell populations in the airway, autoinflammation and autoimmunity, aberrant fibrosis, ac

21 Stat1(-/-)Pdgfrb(+/D849V) ) are rescued from autoinflammation and have improved life span compared wi

22 w that keratinocytes play a key role in skin autoinflammation and identify autophagy modulation of IL

23 s, consistent with the unique association of autoinflammation and immunodeficiency in these patients.

24 roduce TH17 cell subsets as novel players in autoinflammation and thus novel therapeutic targets in a

25 blockade is the treatment of choice for the autoinflammation and vascular manifestations.

26 mutations in CECR1 DADA2 results in variable autoinflammation and vasculopathy (recurrent fevers, liv

27 r cGAS influences the outcome of infections, autoinflammation, and cancer.

28 These findings implicate IL-1-mediated autoinflammation as contributing to the development and

29 We show that the autoinflammation-associated H443P mutant is altered in i

30 ot experiencing clinically overt episodes of autoinflammation at the time of sampling.

31 We also explore the overlap among autoinflammation, autoimmunity and immunodeficiency, and

32 the type I interferonopathies indicates that autoinflammation can be both interferon and noninterfero

33 (ii) autoantigenic stimulation with sterile autoinflammation can lead to tolerance.

34 A patient with multiorgan autoinflammation, combined immunodeficiency, subclinical

35 e spectrum of periodic fever syndromes (PFS)/autoinflammation diseases is continuously expanding.

36 e pathologies including immunodeficiency and autoinflammation in both humans and mice, but microbial

37 The mechanisms that mediate autoinflammation in mevalonate kinase deficiency, a peri

38 ems, and activating mutations in NLRC4 cause autoinflammation in patients.

39 raction between CARD8 and NLRP3 can regulate autoinflammation in patients.

40 tic approach to investigate the mechanism of autoinflammation in Pdgfrb(+/D849V) mice and test the hy

41 me (CAPS) patients with NLRP3 mutations have autoinflammation in skin, joints, and eyes, but not in t

42 This distinguishes it from autoinflammation in which the innate immune system is dy

43 on chain assembly complex (LUBAC), underlies autoinflammation, infections, and amylopectinosis.

44 inherited disorder characterized by chronic autoinflammation, invasive bacterial infections and musc

45 Yet, how IL-10 prevents mucosal autoinflammation is incompletely understood.

46 In this study, we show that the autoinflammation observed in Mefv(V726A/V726A) mice is m

47 h cells are known to be enriched at sites of autoinflammation, our finding that they are highly proin

48 on of actin polymerization leads to systemic autoinflammation that is reduced when IL-18 is deleted b

49 -like cells in the cochlea can mediate local autoinflammation via activation of the NLRP3 inflammasom

50 In this model, autoinflammation was caused by mutation in the actin reg

51 g of the spectrum of organ manifestations in autoinflammation was expanded by the discovery of two no