Effect of anti-interferon-γ and anti-interleukin-2 monoclonal antibody treatment on the development of actively and passively induced experimental allergic encephalomyelitis in the SJL/J mouse

Duong, Trang T.; Louis, Joanne St.; Gilbert, Jeremy; Finkelman, Fred D.; Strejan, Gill H.

doi:10.1016/0165-5728(92)90042-j

Cited by 149 publications

(57 citation statements)

References 29 publications

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“…In addition to antigen or anti-CD3-induced IFN-y production by T (44,45). A similar effect of anti-IFN-y monoclonal antibody was observed in the mouse model of experimental autoimmune uveoretinitis (46 (13)(14)(15)(16)(17).…”

Section: Discussionsupporting

confidence: 50%

Inhibition of T cell responses by activated human CD8+ T cells is mediated by interferon-gamma and is defective in chronic progressive multiple sclerosis.

Balashov

Khoury²,

Hafler³

et al. 1995

J. Clin. Invest.

107

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Section: Discussionsupporting

confidence: 50%

Inhibition of T cell responses by activated human CD8+ T cells is mediated by interferon-gamma and is defective in chronic progressive multiple sclerosis.

Balashov

Khoury²,

Hafler³

et al. 1995

J. Clin. Invest.

107

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“…[31][32][33] IFN-g belongs to a group of proinflammatory cytokines produced by Th1 cells. EAE disease activity, therefore, appears to be determined by more factors than just Th1/Th2 skewing of SP or LN lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

Effect of hematopoietic growth factors on severity of experimental autoimmune encephalomyelitis

Verda

Luo

Kim

et al. 2006

Bone Marrow Transplant

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“…IFN-g-producing Th1 cells were associated with MS lesions (21), and recombinant IFN-g exacerbated disease in MS patients (22). However, in experimental autoimmune encephalomyelitis (EAE), neutralizing IFN-g in vivo (23,24) or targeting the Ifng gene (25,26) or the Ifngr gene (27) increased EAE mortality, whereas intraventricular IFN-g administration suppressed EAE (28).…”

mentioning

confidence: 99%

TheIfngGene Is Essential forVdrGene Expression and Vitamin D3-Mediated Reduction of the Pathogenic T Cell Burden in the Central Nervous System in Experimental Autoimmune Encephalomyelitis, a Multiple Sclerosis Model

Spanier

Nashold

Olson

et al. 2012

The Journal of Immunology

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Compelling evidence suggests that vitamin D3 insufficiency may contribute causally to multiple sclerosis (MS) risk. Experimental autoimmune encephalomyelitis (EAE) research firmly supports this hypothesis. Vitamin D3 supports 1,25-dihydroxyvitamin D3 (1,25-[OH]2D3) synthesis in the CNS, initiating biological processes that reduce pathogenic CD4+ T cell longevity. MS is prevalent in Sardinia despite high ambient UV irradiation, challenging the vitamin D–MS hypothesis. Sardinian MS patients frequently carry a low Ifng expresser allele, suggesting that inadequate IFN-γ may undermine vitamin D3-mediated inhibition of demyelinating disease. Testing this hypothesis, we found vitamin D3 failed to inhibit EAE in female Ifng knockout (GKO) mice, unlike wild-type mice. The two strains did not differ in Cyp27b1 and Cyp24a1 gene expression, implying equivalent vitamin D3 metabolism in the CNS. The 1,25-(OH)2D3 inhibited EAE in both strains, but 2-fold more 1,25-(OH)2D3 was needed in GKO mice, causing hypercalcemic toxicity. Unexpectedly, GKO mice had very low Vdr gene expression in the CNS. Injecting IFN-γ intracranially into adult mice did not increase Vdr gene expression. Correlating with low Vdr expression, GKO mice had more numerous pathogenic Th1 and Th17 cells in the CNS, and 1,25-(OH)2D3 reduced these cells in GKO and wild-type mice without altering Foxp3+ regulatory T cells. Thus, the Ifng gene was needed for CNS Vdr gene expression and vitamin D3-dependent mechanisms that inhibit EAE. Individuals with inadequate Ifng expression may have increased MS risk despite high ambient UV irradiation because of low Vdr gene expression and a high encephalitogenic T cell burden in the CNS.

show abstract

Effect of anti-interferon-γ and anti-interleukin-2 monoclonal antibody treatment on the development of actively and passively induced experimental allergic encephalomyelitis in the SJL/J mouse

Cited by 149 publications

References 29 publications

Inhibition of T cell responses by activated human CD8+ T cells is mediated by interferon-gamma and is defective in chronic progressive multiple sclerosis.

Inhibition of T cell responses by activated human CD8+ T cells is mediated by interferon-gamma and is defective in chronic progressive multiple sclerosis.

Effect of hematopoietic growth factors on severity of experimental autoimmune encephalomyelitis

TheIfngGene Is Essential forVdrGene Expression and Vitamin D3-Mediated Reduction of the Pathogenic T Cell Burden in the Central Nervous System in Experimental Autoimmune Encephalomyelitis, a Multiple Sclerosis Model

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