Ds. Rowbotham et al., PERIPHERAL CELL-MEDIATED IMMUNE-RESPONSE TO MYCOBACTERIAL ANTIGENS ININFLAMMATORY BOWEL-DISEASE, Clinical and experimental immunology, 102(3), 1995, pp. 456-461
A mycobacterial etiology has been proposed in Crohn's disease (CD). We
have sought evidence of increased or modified T lymphocyte immune res
ponses to Mycobacterium tuberculosis and Myco. paratuberculosis in pat
ients with CD (n = 13), compared with ulcerative colitis (UC; n = 17)
and controls (n = 17). Peripheral blood cells were cultured with phyto
haemagglutinin (positive mitogen control), mycobacterial purified prot
ein derivative (PPD) preparations, lysates, column fractions and whole
, heat-killed bacteria. Responses of T cells and T eel subsets were as
sessed by expression of activation markers (CD25, CD69), coupled with
blastogenesis assays (H-3-thymidine uptake) and estimates of prolifera
tion. Virtually all patients responded to Myco. paratuberculosis and M
yco. tuberculosis antigens. There were no significant differences betw
een patient groups, although there was a very high overall correlation
(r = 0.95; P < 0.0001) between responses to the two mycobacterial spe
cies. Most of the activation and proliferative responses resided in th
e CD4(+) (T helper) subset. Although up to 15% of CD8(+) (suppressor/c
ytotoxic) cells also became activated, the CD8(+) cells did not prolif
erate subsequently. Cells expressing the alternate gamma delta form of
the T cell receptor (TCR gamma delta(+)) did not activate or prolifer
ate in response to mycobacterial antigens. There were no differences i
n any of these parameters between patient groups. We conclude that the
re is no specific increase or alteration in cell-mediated anti-mycobac
terial immunity in inflammatory bowel disease (IBD). Thus our data do
not support a mycobacterial etiopathology of Crohn's disease.