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Literature DB >> 19830437

[Interleukin-1 cytokines, inflammasomes, NOD-signalosomes and autoinflammation].

Abstract

The understanding of the genetic and immunological basis of human periodic fever syndromes, in particular cryopyrin-associated periodic syndromes (CAPS), has led to important new insights into the pathogenesis of monogenic and complex interleukin-1beta-associated autoinflammatory diseases. Currently the focus of attention is on the nucleotide-binding oligomerization domain (NOD)-like receptors (NLR), which take part in the regulation of the synthesis and maturation of cytokines in the IL-1 families, NOD-signalosomes and inflammasomes.

Entities: Disease Gene Species

Mesh：

Substances：

Year: 2009 PMID： 19830437 DOI： 10.1007/s00393-009-0488-5

Source DB: PubMed Journal: Z Rheumatol ISSN： 0340-1855 Impact factor: 1.372

79 in total

1. Cytosolic flagellin requires Ipaf for activation of caspase-1 and interleukin 1beta in salmonella-infected macrophages.

Authors: Luigi Franchi; Amal Amer; Mathilde Body-Malapel; Thirumala-Devi Kanneganti; Nesrin Ozören; Rajesh Jagirdar; Naohiro Inohara; Peter Vandenabeele; John Bertin; Anthony Coyle; Ethan P Grant; Gabriel Núñez
Journal: Nat Immunol Date: 2006-04-30 Impact factor: 25.606

2. Converting enzyme-independent release of tumor necrosis factor alpha and IL-1beta from a stimulated human monocytic cell line in the presence of activated neutrophils or purified proteinase 3.

Authors: C Coeshott; C Ohnemus; A Pilyavskaya; S Ross; M Wieczorek; H Kroona; A H Leimer; J Cheronis
Journal: Proc Natl Acad Sci U S A Date: 1999-05-25 Impact factor: 11.205

3. The SPRY domain of Pyrin, mutated in familial Mediterranean fever patients, interacts with inflammasome components and inhibits proIL-1beta processing.

Authors: S Papin; S Cuenin; L Agostini; F Martinon; S Werner; H-D Beer; C Grütter; M Grütter; J Tschopp
Journal: Cell Death Differ Date: 2007-04-13 Impact factor: 15.828

4. Ancient missense mutations in a new member of the RoRet gene family are likely to cause familial Mediterranean fever. The International FMF Consortium.

Authors:
Journal: Cell Date: 1997-08-22 Impact factor: 41.582

5. Activation of inflammasomes requires intracellular redistribution of the apoptotic speck-like protein containing a caspase recruitment domain.

Authors: Nicole B Bryan; Andrea Dorfleutner; Yon Rojanasakul; Christian Stehlik
Journal: J Immunol Date: 2009-03-01 Impact factor: 5.422

6. Early-onset sarcoidosis and CARD15 mutations with constitutive nuclear factor-kappaB activation: common genetic etiology with Blau syndrome.

Authors: Nobuo Kanazawa; Ikuo Okafuji; Naotomo Kambe; Ryuta Nishikomori; Mami Nakata-Hizume; Sonoko Nagai; Akihiko Fuji; Takenosuke Yuasa; Akira Manki; Yoshihiko Sakurai; Mitsuru Nakajima; Hiroko Kobayashi; Ikuma Fujiwara; Hiroyuki Tsutsumi; Atsushi Utani; Chikako Nishigori; Toshio Heike; Tatsutoshi Nakahata; Yoshiki Miyachi
Journal: Blood Date: 2004-09-30 Impact factor: 22.113

7. Therapeutic neutralization of the NLRP1 inflammasome reduces the innate immune response and improves histopathology after traumatic brain injury.

Authors: Juan Pablo de Rivero Vaccari; George Lotocki; Ofelia F Alonso; Helen M Bramlett; W Dalton Dietrich; Robert W Keane
Journal: J Cereb Blood Flow Metab Date: 2009-04-29 Impact factor: 6.200

[Interleukin-1 cytokines, inflammasomes, NOD-signalosomes and autoinflammation].

1. Cytosolic flagellin requires Ipaf for activation of caspase-1 and interleukin 1beta in salmonella-infected macrophages.

2. Converting enzyme-independent release of tumor necrosis factor alpha and IL-1beta from a stimulated human monocytic cell line in the presence of activated neutrophils or purified proteinase 3.

3. The SPRY domain of Pyrin, mutated in familial Mediterranean fever patients, interacts with inflammasome components and inhibits proIL-1beta processing.

4. Ancient missense mutations in a new member of the RoRet gene family are likely to cause familial Mediterranean fever. The International FMF Consortium.

5. Activation of inflammasomes requires intracellular redistribution of the apoptotic speck-like protein containing a caspase recruitment domain.

6. Early-onset sarcoidosis and CARD15 mutations with constitutive nuclear factor-kappaB activation: common genetic etiology with Blau syndrome.

7. Therapeutic neutralization of the NLRP1 inflammasome reduces the innate immune response and improves histopathology after traumatic brain injury.

Review 8. Rilonacept in the treatment of chronic inflammatory disorders.

9. Brain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease.

10. Canakinumab, a fully-human mAb against IL-1beta for the potential treatment of inflammatory disorders.

1. Comorbidities of hidradenitis suppurativa (acne inversa).

Review 2. [Autoinflammatory diseases as cause of wound healing defects].

3. [Comments on the pathogenesis of Behçet's disease. A key to understanding new therapies?].