| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
*
Department of Medical Microbiology and Immunology, Ohio State University College of Medicine and Public Health, Columbus, OH 43210; and
Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110
Oral administration of a myelin component, myelin basic protein
(MBP), induces immunological unresponsiveness to CNS Ags and
ameliorates murine relapsing experimental autoimmune encephalomyelitis
(REAE). However, a recent clinical trial in which multiple sclerosis
patients were treated with repeated doses of oral myelin was
unsuccessful in reducing disease exacerbations. Therefore, we directly
compared the tolerizing capacity of myelin vs MBP during REAE in B10.PL
mice. Oral administration of high doses of myelin, either before
disease induction or during REAE, did not provide protection from
disease or decrease in vitro T cell responses. In contrast, repeated
oral administration of high doses of MBP suppressed established disease
and MBP-specific T cell proliferation and cytokine responses. The
frequency of IL-2-, IFN-
-, and IL-5-secreting MBP-specific T cells
declined with MBP feeding, implicating anergy and/or deletion as the
mechanism(s) of oral tolerance after high Ag doses. We have previously
shown that the dosage and timing of Ag administration are critical
parameters in oral tolerance induction. Studies presented here
demonstrate that Ag homogeneity is also important, i.e., homogeneous Ag
(MBP) is more effective at inducing oral tolerance than heterogeneous
Ag (myelin).
This article has been cited by other articles:
|
|
 |
|
  F. Song, Z. Guan, I. E. Gienapp, T. Shawler, J. Benson, and C. C. Whitacre The Thymus Plays a Role in Oral Tolerance in Experimental Autoimmune Encephalomyelitis J. Immunol., August 1, 2006; 177(3): 1500 - 1509. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Srinivasan, I. E. Gienapp, S. S. Stuckman, C. J. Rogers, S. D. Jewell, P. T. P. Kaumaya, and C. C. Whitacre Suppression of Experimental Autoimmune Encephalomyelitis Using Peptide Mimics of CD28 J. Immunol., August 15, 2002; 169(4): 2180 - 2188. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. B. Jones, D. M. Basso, A. Sodhi, J. Z. Pan, R. P. Hart, R. C. MacCallum, S. Lee, C. C. Whitacre, and P. G. Popovich Pathological CNS Autoimmune Disease Triggered by Traumatic Spinal Cord Injury: Implications for Autoimmune Vaccine Therapy J. Neurosci., April 1, 2002; 22(7): 2690 - 2700. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Maile, B. Wang, W. Schooler, A. Meyer, E. J. Collins, and J. A. Frelinger Antigen-Specific Modulation of an Immune Response by In Vivo Administration of Soluble MHC Class I Tetramers J. Immunol., October 1, 2001; 167(7): 3708 - 3714. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. L. Costa, M. R. Sandora, A. Nakajima, E. V. Nguyen, C. Taylor-Edwards, A. J. Slavin, C. H. Contag, C. G. Fathman, and J. M. Benson Adoptive Immunotherapy of Experimental Autoimmune Encephalomyelitis Via T Cell Delivery of the IL-12 p40 Subunit J. Immunol., August 15, 2001; 167(4): 2379 - 2387. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Srinivasan, R. M. Wardrop, I. E. Gienapp, S. S. Stuckman, C. C. Whitacre, and P. T. P. Kaumaya A Retro-Inverso Peptide Mimic of CD28 Encompassing the MYPPPY Motif Adopts a Polyproline Type II Helix and Inhibits Encephalitogenic T Cells In Vitro J. Immunol., July 1, 2001; 167(1): 578 - 585. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. L. Meyer, J. Benson, F. Song, N. Javed, I. E. Gienapp, J. Goverman, T. A. Brabb, L. Hood, and C. C. Whitacre Rapid Depletion of Peripheral Antigen-Specific T Cells in TCR-Transgenic Mice After Oral Administration of Myelin Basic Protein J. Immunol., May 1, 2001; 166(9): 5773 - 5781. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
