Induction of low dose oral tolerance in IL-10 deficient mice with experimental autoimmune encephalomyelitis
Autor: | Hans Peter Waldner, Patricia A. Gonnella, Howard L. Weiner, Dhatri Kodali |
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Rok vydání: | 2004 |
Předmět: |
medicine.medical_specialty
Encephalomyelitis Autoimmune Experimental Encephalomyelitis medicine.medical_treatment Immunology Administration Oral Biology medicine.disease_cause Autoimmunity Immune tolerance Mice Transforming Growth Factor beta Oral administration Internal medicine Immune Tolerance medicine Animals Immunology and Allergy Cells Cultured Cell Proliferation Glycoproteins Mice Knockout Lamina propria Experimental autoimmune encephalomyelitis Wild type medicine.disease Immunohistochemistry Peptide Fragments Interleukin-10 Mice Inbred C57BL Disease Models Animal medicine.anatomical_structure Endocrinology Cytokine Myelin-Oligodendrocyte Glycoprotein Gene Deletion Spleen |
Zdroj: | Journal of Autoimmunity. 23:193-200 |
ISSN: | 0896-8411 |
DOI: | 10.1016/j.jaut.2004.08.001 |
Popis: | IL-10 has been shown to be an important anti-inflammatory mediator that has both down-regulatory and immunomodulatory effects. Utilizing IL-10(-/-) mice we demonstrate the induction of low dose oral tolerance characterized by the up-regulation of TGF-beta and IL-4 and the suppression of Ag specific proliferation with little suppression of INF-gamma. More severe EAE was found in IL-10(-/-) mice than in wild type controls, however, feeding resulted in amelioration of disease severity in both groups. Orally tolerized IL-10(-/-) mice had greater disease severity compared to orally tolerized wild type mice. IL-4 was present in the GALT of IL-10(-/-) mice and up-regulation of TGF-beta was detected in the lamina propria of fed mice. These results demonstrate that IL-10 is not required for the induction of low dose oral tolerance but is required for the regulation of INF-gamma which affects severity of disease in tolerized mice. |
Databáze: | OpenAIRE |
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