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Induction of oral tolerization in CD86 deficient mice: a role for CD86 and B cells in the up-regulation of TGF-beta.
J Autoimmun. 2006 Mar; 26(2):73-81.JA

Abstract

Feeding myelin oligodendrocyte glycoprotein (MOG) followed by immunization results in induction of oral tolerance evidenced by the amelioration of experimental autoimmune encephalomyelitis (EAE). Oral tolerization is characterized by the suppression of Th1 responses and up-regulation of Th2 responses and TGF-beta. To identify the costimulatory molecules and cell types involved in cytokine-mediated suppression we examined wild type mice and mice deficient for either CD86 (CD86-/-) or B cells (muMT). Oral tolerance was found in CD86-/- mice evidenced by amelioration of disease severity, decreased proliferative responses and IFN-gamma production and increased IL-4. TGF-beta was not up-regulated in CD86-/- or muMT mice but was increased in wild type mice. Analysis of the gut associated lymphoid tissue (GALT) of different mouse strains (C57BL/6 and PLJxSJL F1) fed distinct myelin antigens (MOG and myelin basic protein, MBP) showed that TGF-beta was increased in wild type mice of both strains by 3 days post-immunization and further increased with time. In contrast, no up-regulation of TGF-beta was found in the GALT of CD86-/- or muMT mice. These results demonstrate that CD86 is not required for oral tolerization and that both CD86 and B cells are important for the up-regulation of TGF-beta following oral antigen.

Authors+Show Affiliations

Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. patricia.gonnella@tch.harvard.eduNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16439314

Citation

Gonnella, Patricia A., et al. "Induction of Oral Tolerization in CD86 Deficient Mice: a Role for CD86 and B Cells in the Up-regulation of TGF-beta." Journal of Autoimmunity, vol. 26, no. 2, 2006, pp. 73-81.
Gonnella PA, Chen YH, Waldner H, et al. Induction of oral tolerization in CD86 deficient mice: a role for CD86 and B cells in the up-regulation of TGF-beta. J Autoimmun. 2006;26(2):73-81.
Gonnella, P. A., Chen, Y. H., Waldner, H., & Weiner, H. L. (2006). Induction of oral tolerization in CD86 deficient mice: a role for CD86 and B cells in the up-regulation of TGF-beta. Journal of Autoimmunity, 26(2), 73-81.
Gonnella PA, et al. Induction of Oral Tolerization in CD86 Deficient Mice: a Role for CD86 and B Cells in the Up-regulation of TGF-beta. J Autoimmun. 2006;26(2):73-81. PubMed PMID: 16439314.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Induction of oral tolerization in CD86 deficient mice: a role for CD86 and B cells in the up-regulation of TGF-beta. AU - Gonnella,Patricia A, AU - Chen,Youhai H, AU - Waldner,Hanspeter, AU - Weiner,Howard L, PY - 2004/12/07/received PY - 2005/10/13/revised PY - 2005/10/17/accepted PY - 2006/1/28/pubmed PY - 2006/5/19/medline PY - 2006/1/28/entrez SP - 73 EP - 81 JF - Journal of autoimmunity JO - J. Autoimmun. VL - 26 IS - 2 N2 - Feeding myelin oligodendrocyte glycoprotein (MOG) followed by immunization results in induction of oral tolerance evidenced by the amelioration of experimental autoimmune encephalomyelitis (EAE). Oral tolerization is characterized by the suppression of Th1 responses and up-regulation of Th2 responses and TGF-beta. To identify the costimulatory molecules and cell types involved in cytokine-mediated suppression we examined wild type mice and mice deficient for either CD86 (CD86-/-) or B cells (muMT). Oral tolerance was found in CD86-/- mice evidenced by amelioration of disease severity, decreased proliferative responses and IFN-gamma production and increased IL-4. TGF-beta was not up-regulated in CD86-/- or muMT mice but was increased in wild type mice. Analysis of the gut associated lymphoid tissue (GALT) of different mouse strains (C57BL/6 and PLJxSJL F1) fed distinct myelin antigens (MOG and myelin basic protein, MBP) showed that TGF-beta was increased in wild type mice of both strains by 3 days post-immunization and further increased with time. In contrast, no up-regulation of TGF-beta was found in the GALT of CD86-/- or muMT mice. These results demonstrate that CD86 is not required for oral tolerization and that both CD86 and B cells are important for the up-regulation of TGF-beta following oral antigen. SN - 0896-8411 UR - https://www.unboundmedicine.com/medline/citation/16439314/Induction_of_oral_tolerization_in_CD86_deficient_mice:_a_role_for_CD86_and_B_cells_in_the_up_regulation_of_TGF_beta_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0896-8411(05)00138-1 DB - PRIME DP - Unbound Medicine ER -