Top PDF Delayed onset of experimental autoimmune encephalomyelitis in Olig1 deficient mice.

Delayed onset of experimental autoimmune encephalomyelitis in Olig1 deficient mice.
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EphA4 receptor tyrosine kinase is a modulator of onset and disease severity of experimental autoimmune encephalomyelitis (EAE).
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Baicalin reduces the severity of experimental autoimmune encephalomyelitis
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Ctla-4 modulates the differentiation of inducible Foxp3+ Treg cells but IL-10 mediates their function in experimental autoimmune encephalomyelitis.
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Partial deficiency of sphingosine-1-phosphate lyase confers protection in experimental autoimmune encephalomyelitis.
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Amelioration of experimental autoimmune encephalomyelitis in C57BL/6 mice by photobiomodulation induced by 670 nm light.
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GCN2 kinase plays an important role triggering the remission phase of experimental autoimmune encephalomyelitis (EAE) in mice
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Hsp70 regulates immune response in experimental autoimmune encephalomyelitis.
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Chloroquine treatment enhances regulatory T cells and reduces the severity of experimental autoimmune encephalomyelitis.
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Protoporphyrin Treatment Modulates Susceptibility to Experimental Autoimmune Encephalomyelitis in miR-155-Deficient Mice.
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Kinin B(2) receptor regulates chemokines CCL2 and CCL5 expression and modulates leukocyte recruitment and pathology in experimental autoimmune encephalomyelitis (EAE) in mice
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Regulatory T cell induction during Plasmodium chabaudi infection modifies the clinical course of experimental autoimmune encephalomyelitis.
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Cathepsin B in antigen-presenting cells controls mediators of the Th1 immune response during Leishmania major infection.
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Altered hematopoiesis in mice lacking DNA polymerase mu is due to inefficient double-strand break repair.
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HVEM signalling promotes colitis.
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Decreased production of TNF-alpha by lymph node cells indicates experimental autoimmune encephalomyelitis remission in Lewis rats
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Rev. bras. farmacogn. vol.22 número3
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Age-related retinopathy in NRF2-deficient mice.
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BCG and BCG/DNAhsp65 Vaccinations Promote Protective Effects without Deleterious Consequences for Experimental Autoimmune Encephalomyelitis
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Increased autoimmune diabetes in pIgR-deficient NOD mice is due to a "Hitchhiking" interval that refines the genetic effect of Idd5.4.
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