IL-36 signaling amplifies Th1 responses by enhancing proliferation and Th1 polarization of naive CD4+ T cells

被引：209

作者：

Vigne, Solenne ^{[1
,2
]}

Palmer, Gaby ^{[1
,2
]}

Martin, Praxedis ^{[1
,2
]}

Lamacchia, Celine ^{[1
,2
]}

Strebel, Deborah ^{[1
,2
]}

Rodriguez, Emiliana ^{[1
,2
]}

Oileros, Maria L. ^{[2
]}

Vesin, Dominique ^{[2
]}

Garcia, Irene ^{[2
]}

Ronchi, Francesca ^{[3
]}

Sallusto, Federica ^{[3
]}

Sims, John E. ^{[4
]}

Gabay, Cem ^{[1
,2
]}

机构：

[1] Univ Geneva, Sch Med, Dept Internal Med, Div Rheumatol, CH-1211 Geneva, Switzerland

[2] Univ Geneva, Sch Med, Dept Pathol Immunol, CH-1211 Geneva, Switzerland

[3] Inst Res Biomed, Bellinzona, Switzerland

[4] Amgen Inc, Dept Inflammat Res, Seattle, WA USA

来源：

BLOOD | 2012年 / 120卷 / 17期

基金：

瑞士国家科学基金会;

关键词：

GENERALIZED PUSTULAR PSORIASIS; INFLAMMATORY SKIN-DISEASE; BACILLUS-CALMETTE-GUERIN; NF-KAPPA-B; MYCOBACTERIUM-TUBERCULOSIS; FAMILY CYTOKINES; HOST-DEFENSE; INFECTION; MEMBERS; RECEPTOR;

D O I：

10.1182/blood-2012-06-439026

中图分类号：

R5 [内科学];

学科分类号：

100201 [内科学];

摘要：

The interleukin-1 (IL-1) superfamily of cytokines comprises a set of pivotal mediators of inflammation. Among them, the action of IL-36 cytokines in immune responses has remained elusive. In a recent study, we demonstrated a direct effect of IL-36 on immune cells. Here we show that, among T cells, the IL-36 receptor is predominantly expressed on naive CD4(+) T cells and that IL-36 cytokines act directly on naive T cells by enhancing both cell proliferation and IL-2 secretion. IL-36 beta acts in synergy with IL-12 to promote Th1 polarization and IL-36 signaling is also involved in mediating Th1 immune responses to Bacillus Calmette-Guerin infection in vivo. Our findings point toward a critical function of IL-36 in the priming of Th1 cell responses in vitro, and in adaptive immunity in a model of mycobacterial infection in vivo. (Blood. 2012;120(17):3478-3487)

引用

页码：3478 / 3487

页数：10

共 41 条

[1]

Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of interleukin 17-producing human T helper cells [J].

Acosta-Rodriguez, Eva V. ;

Napolitani, Giorgio ;

Lanzavecchia, Antonio ;

Sallusto, Federica .

NATURE IMMUNOLOGY, 2007, 8 (09) :942-949

[2]

IL-1, IL-18, and IL-33 families of cytokines [J].

Arend, William P. ;

Palmer, Gaby ;

Gabay, Cem .

IMMUNOLOGICAL REVIEWS, 2008, 223 :20-38

[3]

Opposing activities of two novel members of the IL-1 ligand family regulate skin inflammation [J].

Blumberg, Hal ;

Dinh, Huyen ;

Trueblood, Esther S. ;

Pretorius, James ;

Kugler, David ;

Weng, Ning ;

Kanaly, Suzanne T. ;

Towne, Jennifer E. ;

Willis, Cynthia R. ;

Kuechle, Melanie K. ;

Sims, John E. ;

Peschon, Jacques J. .

JOURNAL OF EXPERIMENTAL MEDICINE, 2007, 204 (11) :2603-2614

[4]

IL-1RL2 and Its Ligands Contribute to the Cytokine Network in Psoriasis [J].

Blumberg, Hal ;

Dinh, Huyen ;

Dean, Charles, Jr. ;

Trueblood, Esther S. ;

Bailey, Keith ;

Shows, Donna ;

Bhagavathula, Narasimharao ;

Aslam, Muhammad Nadeem ;

Varani, James ;

Towne, Jennifer E. ;

Sims, John E. .

JOURNAL OF IMMUNOLOGY, 2010, 185 (07) :4354-4362

[5]

A distal region in the interferon-γ gene is a site of epigenetic remodeling and transcriptional regulation by interleukin-2 [J].

Bream, JH ;

Hodge, DL ;

Gonsky, R ;

Spolski, R ;

Leonard, WJ ;

Krebs, S ;

Targan, S ;

Morinobu, A ;

O'Shea, JJ ;

Young, HA .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (39) :41249-41257

[6]

Inter-Regulation of Th17 Cytokines and the IL-36 Cytokines In Vitro and In Vivo: Implications in Psoriasis Pathogenesis [J].

Carrier, Yijun ;

Ma, Hak-Ling ;

Ramon, Hilda E. ;

Napierata, Lee ;

Small, Clayton ;

O'Toole, Margot ;

Young, Deborah A. ;

Fouser, Lynette A. ;

Nickerson-Nutter, Cheryl ;

Collins, Mary ;

Dunussi-Joannopoulos, Kyri ;

Medley, Quintus G. .

JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2011, 131 (12) :2428-2437

[7]

Critical Regulation of Early Th17 Cell Differentiation by Interleukin-1 Signaling [J].

Chung, Yeonseok ;

Chang, Seon Hee ;

Martinez, Gustavo J. ;

Yang, Xuexian O. ;

Nurieva, Roza ;

Kang, Hong Soon ;

Ma, Li ;

Watowich, Stephanie S. ;

Jetten, Anton M. ;

Tian, Qiang ;

Dong, Chen .

IMMUNITY, 2009, 30 (04) :576-587

[8]

Two novel IL-1 family members, IL-1δ and IL-1ε, function as an antagonist and agonist of NF-κB activation through the orphan IL-1 receptor-related protein 2 [J].

Debets, R ;

Timans, JC ;

Homey, B ;

Zurawski, S ;

Sana, TR ;

Lo, S ;

Wagner, J ;

Edwards, G ;

Clifford, T ;

Menon, S ;

Bazan, JF ;

Kastelein, RA .

JOURNAL OF IMMUNOLOGY, 2001, 167 (03) :1440-1446

[9]

IL-1 family nomenclature [J].

Dinarello, Charles ;

Arend, William ;

Sims, John ;

Smith, Dirk ;

Blumberg, Hal ;

O'Neill, Luke ;

Goldbach-Mansky, Raphaela ;

Pizarro, Theresa ;

Hoffman, H. ;

Bufler, Philip ;

Nold, Marcel ;

Ghezzi, Pietro ;

Mantovani, Alberto ;

Garlanda, Cecilia ;

Boraschi, Diana ;

Rubartelli, Anna ;

Netea, Mihai ;

van der Meer, Jos ;

Joosten, Leo ;

Mandrup-Poulsen, Tom ;

Donath, Marc ;

Lewis, Eli ;

Pfeilschifter, Josef ;

Martin, Michael ;

Kracht, Michael ;

Muehl, H. ;

Novick, Daniela ;

Lukic, Miodrag ;

Conti, Bruno ;

Solinger, Alan ;

Peyman, Kelk ;

van de Veerdonk, Frank ;

Gabel, Chiristopher .

NATURE IMMUNOLOGY, 2010, 11 (11) :973-973

[10]

IL-1 pathways in inflammation and human diseases [J].

Gabay, Cem ;

Lamacchia, Celine ;

Palmer, Gaby .

NATURE REVIEWS RHEUMATOLOGY, 2010, 6 (04) :232-241

← 1 2 3 4 5 →