These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Autoimmune uveitis and antigenic mimicry of environmental antigens.
    Author: Wildner G, Diedrichs-Möhring M.
    Journal: Autoimmun Rev; 2004 Jul; 3(5):383-7. PubMed ID: 15288005.
    Abstract:
    Autoimmunity directed against antigens of immune privileged sites, which are hidden from the immune system by blood-organ-barriers, is difficult to explain: it would require already activated cells to enter the tissue where the respective autoantigens are sequestered. Autoimmune uveitis, a sight-threatening inflammatory disease of the eye, is such an example. To induce disease autoreactive T cells must have been activated outside the eye to pass the blood-retina-barrier and then crossreact with retinal autoantigen. We have described two environmental peptides mimicking a highly pathogenic epitope from retinal S-antigen. One mimicry antigen is from rotavirus, a common pathogen causing gastroenteritis, the other from bovine milk alpha s2casein, a frequent nutritional protein ought to induce oral tolerance. Lewis rats develop uveitis after immunization with both mimicry peptides and casein protein. However, these mimicry antigens failed to induce oral tolerance for protection from uveitis, suspecting that they rather induce immunity than tolerance. Humoral and cellular immune responses to these antigens are enhanced and more frequent in patients with uveitis compared to healthy individuals. Our findings suggest that multiple environmental antigens mimic autoantigens and might cause autoimmune diseases by eliciting defensive immune responses, however, they are not necessarily useful for therapeutic tolerance induction.
    [Abstract] [Full Text] [Related] [New Search]