Regulation and function of interleukin-36 cytokines

被引：187

作者：

Bassoy, Esen Yonca ^{[1
,2
,3
]}

Towne, Jennifer E. ^{[4
]}

Gabay, Cem ^{[1
,2
,3
]}

机构：

[1] Univ Hosp Geneva, Dept Internal Med Specialties, Div Rheumatol, Geneva, Switzerland

[2] Univ Hosp Geneva, Dept Pathol Immunol, Geneva, Switzerland

[3] Univ Geneva, Geneva, Switzerland

[4] Janssen Res & Dev, Immunol Discovery, San Diego, CA 92121 USA

来源：

IMMUNOLOGICAL REVIEWS | 2018年 / 281卷 / 01期

基金：

瑞士国家科学基金会;

关键词：

IL-1; family; inflammation; intestine; lung; psoriasis; GENERALIZED PUSTULAR PSORIASIS; BRONCHIAL EPITHELIAL-CELLS; IL-36 RECEPTOR ANTAGONIST; SKIN INFLAMMATION; AP1S3; MUTATIONS; FAMILY-MEMBERS; T-LYMPHOCYTES; MYELOID CELLS; EXPRESSION; ACTIVATION;

D O I：

10.1111/imr.12610

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

The interleukin (IL)-36 cytokines include 3 agonists, IL-36, IL-36, and IL-36 that bind to a common receptor composed of IL-36R and IL-1RAcP to stimulate inflammatory responses. IL-36Ra is a natural antagonist that binds to IL-36R, but does not recruit the co-receptor IL-1RAcP and does not stimulate any intracellular responses. The IL-36 cytokines are expressed predominantly by epithelial cells and act on a number of cells including immune cells, epithelial cells, and fibroblasts. Processing of the N-terminus is required for full agonist or antagonist activity for all IL-36 members. The role of IL-36 has been extensively demonstrated in the skin where it can act on keratinocytes and immune cells to induce a robust inflammatory response that has been implicated in psoriatic disorders. Emerging data also suggest a role for this cytokine family in pulmonary and intestinal physiology and pathology.

引用

页码：169 / 178

页数：10

共 87 条

[41]

Cutting edge:: Opposite effects of IL-1 and IL-2 on the regulation of IL-17+ T cell pool IL-1 subverts IL-2-mediated suppression [J].

Kryczek, Ilona ;

Wei, Shuang ;

Vatan, Linhua ;

Escara-Wilke, June ;

Szeliga, Wojciech ;

Keller, Evan T. ;

Zou, Weiping .

JOURNAL OF IMMUNOLOGY, 2007, 179 (03) :1423-1426

[42]

The severity of experimental arthritis is independent of IL-36 receptor signaling [J].

Lamacchia, Celine ;

Palmer, Gaby ;

Rodriguez, Emiliana ;

Martin, Praxedis ;

Vigne, Solenne ;

Seemayer, Christian A. ;

Talabot-Ayer, Dominique ;

Towne, Jennifer E. ;

Gabay, Cem .

ARTHRITIS RESEARCH & THERAPY, 2013, 15 (02)

[43]

Role of IL-1 Beta in the Development of Human TH17 Cells: Lesson from NLPR3 Mutated Patients [J].

Lasiglie, Denise ;

Traggiai, Elisabetta ;

Federici, Silvia ;

Alessio, Maria ;

Buoncompagni, Antonella ;

Accogli, Andrea ;

Chiesa, Sabrina ;

Penco, Federica ;

Martini, Alberto ;

Gattorno, Marco .

PLOS ONE, 2011, 6 (05)

[44]

The Double-Stranded RNA Analogue Polyinosinic-Polycytidylic Acid Induces Keratinocyte Pyroptosis and Release of IL-36γ [J].

Lian, Li-Hua ;

Milora, Katelynn A. ;

Manupipatpong, Katherine K. ;

Jensen, Liselotte E. .

JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2012, 132 (05) :1346-1353

[45]

Mutations in IL36RN are associated with geographic tongue [J].

Liang, Jianying ;

Huang, Peichen ;

Li, Huaguo ;

Zhang, Jia ;

Ni, Cheng ;

Wang, Yirong ;

Shen, Jinwen ;

Li, Chunxiao ;

Kang, Lu ;

Chen, Jie ;

Zhang, Hui ;

Wang, Zhen ;

Zhang, Zhen ;

Li, Ming ;

Yao, Zhirong .

HUMAN GENETICS, 2017, 136 (02) :241-252

[46]

Neutrophil Elastase-mediated proteolysis activates the anti-inflammatory cytokine IL-36 Receptor antagonist [J].

Macleod, Tom ;

Doble, Rosella ;

McGonagle, Dennis ;

Wasson, Christopher W. ;

Alase, Adewonuola ;

Stacey, Martin ;

Wittmann, Miriam .

SCIENTIFIC REPORTS, 2016, 6

[47]

The new IL-1 family member IL-1F8 stimulates production of inflammatory mediators by synovial fibroblasts and articular chondrocytes [J].

Magne, David ;

Palmer, Gaby ;

Barton, Jenny L. ;

Mezin, Francoise ;

Talabot-Ayer, Dominique ;

Bas, Sylvette ;

Duffy, Trevor ;

Noger, Marcus ;

Guerne, Pierre-Andre ;

Nicklin, Martin J. H. ;

Gabay, Cem .

ARTHRITIS RESEARCH & THERAPY, 2006, 8 (03)

[48]

AP1S3 Mutations Cause Skin Autoinflammation by Disrupting Keratinocyte Autophagy and Up-Regulating IL-36 Production [J].

Mahil, Satveer K. ;

Twelves, Sophie ;

Farkas, Katalin ;

Setta-Kaffetzi, Niovi ;

Burden, A. David ;

Gach, Joanna E. ;

Irvine, Alan D. ;

Kepiro, Laszlo ;

Mockenhaupt, Maja ;

Oon, Hazel H. ;

Pinner, Jason ;

Ranki, Annamari ;

Seyger, Marieke M. B. ;

Soler-Palacin, Pere ;

Storan, Eoin R. ;

Tan, Eugene S. ;

Valeyrie-Allanore, Laurence ;

Young, Helen S. ;

Trembath, Richard C. ;

Choon, Siew-Eng ;

Szell, Marta ;

Bata-Csorgo, Zsuzsanna ;

Smith, Catherine H. ;

Di Meglio, Paola ;

Barker, Jonathan N. ;

Capon, Francesca .

JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2016, 136 (11) :2251-2259

[49]

Interleukin-36-Receptor Antagonist Deficiency and Generalized Pustular Psoriasis [J].

Marrakchi, Slaheddine ;

Guigue, Philippe ;

Renshaw, Blair R. ;

Puel, Anne ;

Pei, Xue-Yuan ;

Fraitag, Sylvie ;

Zribi, Jihen ;

Bal, Elodie ;

Cluzeau, Celine ;

Chrabieh, Maya ;

Towne, Jennifer E. ;

Douangpanya, Jason ;

Pons, Christian ;

Mansour, Sourour ;

Serre, Valerie ;

Makni, Hafedh ;

Mahfoudh, Nadia ;

Fakhfakh, Faiza ;

Bodemer, Christine ;

Feingold, Josue ;

Hadj-Rabia, Smail ;

Favre, Michel ;

Genin, Emmanuelle ;

Sahbatou, Mourad ;

Munnich, Arnold ;

Casanova, Jean-Laurent ;

Sims, John E. ;

Turki, Hamida ;

Bachelez, Herve ;

Smahi, Asma .

NEW ENGLAND JOURNAL OF MEDICINE, 2011, 365 (07) :620-628

[50]

The balance between pro- and anti-inflammatory cytokines is crucial in human allergic contact dermatitis pathogenesis: the role of IL-1 family members [J].

Mattii, Martina ;

Ayala, Fabio ;

Balato, Nicola ;

Filotico, Raffaele ;

Lembo, Serena ;

Schiattarella, Maria ;

Patruno, Cataldo ;

Marone, Gianni ;

Balato, Anna .

EXPERIMENTAL DERMATOLOGY, 2013, 22 (12) :813-819

← 1 2 3 4 5 6 7 8 9 →