|Olsen, Ingrid - National Veterinary Institute - Norway|
|Tollefsen, Stig - National Veterinary Institute - Norway|
|Aagaard, Claus - National Veterinary Institute - Norway|
|Reitan, Liv - National Veterinary Institute - Norway|
|Andersen, Peter - Staten Serum Institute|
|Sollid, Ludvig - National Veterinary Institute - Norway|
|Lundin, Knut - National Veterinary Institute - Norway|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 8/9/2009
Publication Date: 8/9/2009
Citation: Olsen, I., Tollefsen, S., Aagaard, C., Reitan, L.J., Bannantine, J.P., Andersen, P., Sollid, L.M., Lundin, K.E. 2009. CD4 T Cells From Intestinal Biopsies of Crohn's Disease Patients React to Mycobacterium avium subspecies paratuberculosis [abstract].
Technical Abstract: The role of Mycobacterium avium subspecies paratuberculosis (MAP) in Crohn’s disease (CD) remains controversial. One issue that has been raised is the lack of data showing a cellular immune response to MAP. Earlier studies have mostly focused on responses in peripheral blood which have several limitations. We thus wanted to characterize the response in the affected tissue and consequently made T-cell lines from intestinal biopsies of patients with CD (n=11), ulcerative colitis (UC) (n=13) and controls (n=10). The T cells from CD patients showed higher proliferation in response to MAP compared to UC patients (p<0.025), while no differences were detected in response to commensal bacteria. T-cells clones (n= 28) were made from four CD patients and tested for responses to various mycobacterial species. One T-cell clone responded only to MAP and the very closely related M. avium subspecies avium (MAA) while another responded to MAP, MAA and Mycobacterium intracellulare. A more broadly reactive T-cell clone reacted to MAP1508 which belongs to esx family. The T-cell clones produced IFN-gamma and/or IL-17 but minimal amounts of IL-4. The presence of MAP responsive T cells producing proinflammatory cytokines suggests that MAP may contribute to the pathogenesis of CD.