TY - JOUR
T1 - Interleukin 4 deficiency limits the development of a lupus-like disease in mice triggered by phospholipids in a non-bilayer arrangement
AU - Reséndiz-Mora, Albany
AU - Wong-Baeza, Carlos
AU - Nevárez-Lechuga, Irene
AU - Landa-Saldívar, Carla
AU - Molina-Gómez, Eréndira
AU - Hernández-Pando, Rogelio
AU - Wong-Baeza, Isabel
AU - Escobar-Gutiérrez, Alejandro
AU - Baeza, Isabel
N1 - Publisher Copyright:
© 2020 The Scandinavian Foundation for Immunology
PY - 2021/3
Y1 - 2021/3
N2 - Non-bilayer phospholipids arrangements (NPAs) are transient molecular associations different from lipid bilayers. When they become stable, they can trigger a disease in mice resembling human lupus, which is mainly characterized by the production of anti-NPA IgG antibodies. NPAs are stabilized on liposomes or cell bilayers by the drugs procainamide or chlorpromazine, which produce drug-induced lupus in humans. Here, we evaluated the participation of the TH2 response, through its hallmark cytokine IL-4, on the development of the lupus-like disease in mice. Wild-type or IL-4 knockout BALB/c mice received liposomes bearing drug-induced NPAs, the drugs alone, or an anti-NPA monoclonal antibody (H308) to induce the lupus-like disease (the last two procedures stabilize NPAs on mice cells). IL-4 KO mice showed minor disease manifestations, compared to wild-type mice, with decreased production of anti-NPA IgG antibodies, no anti-cardiolipin, anti-histones and anticoagulant antibodies, and no kidney or skin lesions. In these mice, H308 was the only inducer of anti-NPA IgG antibodies. These findings indicate that IL-4 has a central role in the development of the murine lupus-like disease induced by NPA stabilization.
AB - Non-bilayer phospholipids arrangements (NPAs) are transient molecular associations different from lipid bilayers. When they become stable, they can trigger a disease in mice resembling human lupus, which is mainly characterized by the production of anti-NPA IgG antibodies. NPAs are stabilized on liposomes or cell bilayers by the drugs procainamide or chlorpromazine, which produce drug-induced lupus in humans. Here, we evaluated the participation of the TH2 response, through its hallmark cytokine IL-4, on the development of the lupus-like disease in mice. Wild-type or IL-4 knockout BALB/c mice received liposomes bearing drug-induced NPAs, the drugs alone, or an anti-NPA monoclonal antibody (H308) to induce the lupus-like disease (the last two procedures stabilize NPAs on mice cells). IL-4 KO mice showed minor disease manifestations, compared to wild-type mice, with decreased production of anti-NPA IgG antibodies, no anti-cardiolipin, anti-histones and anticoagulant antibodies, and no kidney or skin lesions. In these mice, H308 was the only inducer of anti-NPA IgG antibodies. These findings indicate that IL-4 has a central role in the development of the murine lupus-like disease induced by NPA stabilization.
KW - IL-4
KW - non-bilayer phospholipid arrangements
KW - systemic lupus erythematosus
UR - http://www.scopus.com/inward/record.url?scp=85097996336&partnerID=8YFLogxK
U2 - 10.1111/sji.13002
DO - 10.1111/sji.13002
M3 - Artículo
C2 - 33247472
AN - SCOPUS:85097996336
SN - 0300-9475
VL - 93
JO - Scandinavian Journal of Immunology
JF - Scandinavian Journal of Immunology
IS - 3
M1 - e13002
ER -