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Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
immunology and microbiology
IFN-γ deficiency exacerbates experimental autoimmune neuritis in mice despite a mitigated systemic Th1 immune response
Journal of Neuroimmunology, Volume 246, No. 1-2, Year 2012
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Description
Previous studies have shown that interferon-gamma (IFN-γ) is a proinflammatory cytokine that contributes to the pathogenesis of Guillain-Barré syndrome and its animal model, experimental autoimmune neuritis (EAN). Treatments with anti-IFN-γ antibodies improve clinical outcome in GBS patients and EAN animals and administration of IFN-γ markedly worsens EAN. Paradoxically, the mice deficient in IFN-γ remain susceptible to experimental autoimmune encephalomyelitis, an analogous disease in the central nervous system. These observations raise a question whether IFN-γ might be protective in autoimmune demyelinating diseases. To clarify the role of IFN-γ in the pathogenesis of autoimmune demyelinating diseases, we used P0 protein peptide 180-199 to induce EAN in IFN-γ knockout (KO) mice. After the acute phase of EAN, the clinical signs of IFN-γ KO mice were significantly more severe than those of wild type (WT) controls. After antigenic stimulation, the proliferation of splenic mononuclear cells was significantly higher in IFN-γ KO than in WT mice with EAN. At the peak of EAN, the proportion of interleukin (IL)-17A expressing cells in cauda equina (CE) infiltrating cells, and the levels of IL-17A in sera were elevated in IFN-γ KO mice when compared with their WT counterparts. The proportions of major histocompatibility complex (MHC) II, macrosialin, and IL-12/IL-23p40 expressing cells, relative to total CE infiltrating cells were correspondingly higher in IFN-γ KO than in WT mice with EAN. However, IFN-γ deficiency reduced the production of NO by cultured macrophages in response to proinflammatory stimuli and induced a systemic Th2-oriented immune response. In conclusion, IFN-γ deficiency exacerbates EAN via upregulating Th17 cells despite a mitigated systemic Th1 immune response. © 2012 Elsevier B.V.
Authors & Co-Authors
Zhang, Hong Liang
Sweden, Stockholm
Karolinska Institutet
Sheikh, Azimullah
United Arab Emirates, Al Ain
United Arab Emirates University
Zheng, Xiang Yu
Sweden, Stockholm
Karolinska Institutet
Wang, Xiao Ke
Sweden, Stockholm
Karolinska Institutet
China, Changchun
The Second Hospital of Jilin University
Amir, Naheed
United Arab Emirates, Al Ain
United Arab Emirates University
Mensah-Brown, Eric P.K.
United Arab Emirates, Al Ain
United Arab Emirates University
Al-Shamsi, Mariam S.
United Arab Emirates, Al Ain
United Arab Emirates University
Shahin, Allen
United Arab Emirates, Al Ain
United Arab Emirates University
Press, Rayomand
Sweden, Stockholm
Karolinska Universitetssjukhuset
Zhu, Jie
Sweden, Stockholm
Karolinska Institutet
China, Changchun
The First Bethune Hospital of Jilin University
Adem, Abdu
United Arab Emirates, Al Ain
United Arab Emirates University
Statistics
Citations: 30
Authors: 11
Affiliations: 5
Identifiers
Doi:
10.1016/j.jneuroim.2012.02.011
ISSN:
01655728
e-ISSN:
18728421