Autoantibodies against IL-17A, IL-17F, and IL-22 in patients with chronic mucocutaneous candidiasis and autoimmune polyendocrine syndrome type I

被引：533

作者：

Puel, Anne ^{[1
,2
]}

Doeffinger, Rainer ^{[3
]}

Natividad, Angels ^{[1
,2
]}

Chrabieh, Maya ^{[1
,2
]}

Barcenas-Morales, Gabriela ^{[4
]}

Picard, Capucine ^{[1
,2
,5
]}

Cobat, Aurelie ^{[1
,2
]}

Ouachee-Chardin, Marie ^{[8
]}

Toulon, Antoine ^{[2
,6
]}

Bustamante, Jacinta ^{[1
,2
]}

Al-Muhsen, Saleh ^{[9
]}

Al-Owain, Mohammed ^{[10
]}

Arkwright, Peter D. ^{[11
]}

Costigan, Colm ^{[12
]}

McConnell, Vivienne ^{[13
]}

Cant, Andrew J. ^{[14
]}

Abinun, Mario ^{[14
]}

Polak, Michel ^{[2
,15
]}

Bougneres, Pierre-Francois ^{[16
]}

Kumararatne, Dinakantha ^{[3
]}

Marodi, Laszlo ^{[17
,18
]}

Nahum, Amit ^{[19
,20
]}

Roifman, Chaim ^{[19
,20
]}

Blanche, Stephane ^{[2
,7
]}

Fischer, Alain ^{[2
,7
,21
]}

Bodemer, Christine ^{[2
,6
]}

Abel, Laurent ^{[1
,2
,22
]}

Lilic, Desa ^{[23
]}

Casanova, Jean-Laurent ^{[1
,2
,7
,22
]}

机构：

[1] INSERM, U550, Lab Human Genet Infect Dis, Necker Branch, F-75015 Paris, France

[2] Univ Paris 05, Necker Med Sch, F-75015 Paris, France

[3] Addenbrookes Hosp, Dept Clin Biochem & Immunol, Cambridge CB2 0QQ, England

[4] Univ Nacl Autonoma Mexico, Immunol Lab, Fac Estudios Super Cuautitlan, Izcalli 54700, Edo De Mexico, Mexico

[5] Hop Necker Enfants Malad, AP HP, Study Ctr Primary Immunodeficiencies, F-75015 Paris, France

[6] Hop Necker Enfants Malad, AP HP, Dermatol Unit, F-75015 Paris, France

[7] Hop Necker Enfants Malad, AP HP, Pediat Hematol Immunol Unit, F-75015 Paris, France

[8] Hop Robert Debre, Pediat Hematol Unit, F-75019 Paris, France

[9] King Saud Univ, Coll Med, Dept Pediat, Novel Primary Immunodeficiency & Infect Dis Progr, Riyadh 11451, Saudi Arabia

[10] King Faisal Specialist Hosp & Res Ctr, Dept Med Genet, Riyadh 11211, Saudi Arabia

[11] Univ Manchester, Dept Paediat Allergy & Immunol, Royal Manchester Childrens Hosp, Manchester M13 9WP, Lancs, England

[12] Our Ladys Hosp Sick Children, Dublin 12, Ireland

[13] Belfast City Hosp, No Ireland Reg Genet Serv, Belfast BT9 7AB, Antrim, North Ireland

[14] Newcastle Upon Tyne Hosp, NHS Fdn Trust, Dept Paediat Immunol, Newcastle Upon Tyne NE4 6BE, Tyne & Wear, England

[15] Pediat Endocrinol Necker Hosp, INSERM, U845, Lab Normal & Pathol Dev Endocrine Organs, F-75015 Paris, France

[16] Hop St Vincent de Paul, F-75014 Paris, France

[17] Univ Debrecen, Dept Infect & Pediat Immunol, H-4032 Debrecen, Hungary

[18] Hlth Sci Ctr, H-4032 Debrecen, Hungary

[19] Hosp Sick Children, Dept Paediat, Div Immunol & Allergy, Toronto, ON M5G 1X8, Canada

[20] Univ Toronto, Toronto, ON M5G 1X8, Canada

[21] INSERM, U768, Lab Normal & Pathol Dev Immune Syst, F-75015 Paris, France

[22] Rockefeller Univ, Lab Human Genet Infect Dis, Rockefeller Branch, New York, NY 10065 USA

[23] Univ Newcastle, Inst Cellular Med, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England

来源：

JOURNAL OF EXPERIMENTAL MEDICINE | 2010年 / 207卷 / 02期

基金：

匈牙利科学研究基金会;

关键词：

HYPER-IGE SYNDROME; PULMONARY ALVEOLAR PROTEINOSIS; TH17; CELLS; IFN-GAMMA; CLINICAL-MANIFESTATIONS; INBORN-ERRORS; HOST-DEFENSE; T-CELLS; IMMUNITY; MUTATIONS;

D O I：

10.1084/jem.20091983

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Most patients with autoimmune polyendocrine syndrome type I (APS-I) display chronic mucocutaneous candidiasis (CMC). We hypothesized that this CMC might result from autoimmunity to interleukin (IL)-17 cytokines. We found high titers of autoantibodies (auto-Abs) against IL-17A, IL-17F, and/or IL-22 in the sera of all 33 patients tested, as detected by multiplex particle-based flow cytometry. The auto-Abs against IL-17A, IL-17F, and IL-22 were specific in the five patients tested, as shown by Western blotting. The auto-Abs against IL-17A were neutralizing in the only patient tested, as shown by bioassays of IL-17A activity. None of the 37 healthy controls and none of the 103 patients with other autoimmune disorders tested had such auto-Abs. None of the patients with APS-I had auto-Abs against cytokines previously shown to cause other well-defined clinical syndromes in other patients (IL-6, interferon [IFN]-gamma, or granulocyte/macrophage colony-stimulating factor) or against other cytokines (IL-1 beta, IL-10, IL-12, IL-18, IL-21, IL-23, IL-26, IFN-beta, tumor necrosis factor [alpha], or transforming growth factor beta). These findings suggest that auto-Abs against IL-17A, IL-17F, and IL-22 may cause CMC in patients with APS-I.

引用

页码：291 / 297

页数：7

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