Interferon-gamma and interleukin-2 release by lymphocytes derived from theblood, mesenteric lymph nodes and intestines of normal sheep and those affected with paratuberculosis (Johne's disease)
C. Burrells et al., Interferon-gamma and interleukin-2 release by lymphocytes derived from theblood, mesenteric lymph nodes and intestines of normal sheep and those affected with paratuberculosis (Johne's disease), VET IMMUNOL, 68(2-4), 1999, pp. 139-148
This study sought to determine if T-cell cytokine responses to mycobacteria
l infections in sheep were similar to those in other species and if such re
sponses correlated with prevailing gut pathology. Lymphocytes were isolated
from the blood (PBL), mesenteric lymph nodes (MLN) and ileal lamina propri
a (LPL) of control sheep and of sheep with clinical Johne's disease due to
infection with Mycobacterium avium ssp. paratuberculosis (M.a. paratubercul
osis). These animals had previously been categorised into two,groups exhibi
ting either the 'tuberculoid' (paucibacillary) form of lesion or the 'lepro
matous' (multibacillary) form. Lymphocytes were examined for their capacity
, following stimulation with johnin-PPD, to release interferon-gamma (IFN-g
amma) and interleukin 2 (IL-2) characteristic of the Th1 subset of MHC Clas
s II-restricted CD4(+) (helper) T-cells in other species. The expression of
the two cytokines appeared related to the type of histological lesion obse
rved. Antigen-stimulated lymphocytes from the tuberculoid group exhibited g
reater release of IFN-gamma and IL-2 than lymphocytes from the lepromatous
group suggesting a Th1-type of response in the former in which expression o
f IFN-gamma by PBL showed a significant positive correlation with that expr
essed by MLN and LPL. Lymphocytes from animals with lepromatous lesions rel
eased lesser mycobacterium-induced IFN-gamma and IL-2 indicating a diminish
ed role for a Th1 subset in this group of sheep. Differences in cytokine ex
pression were much more apparent with lymphocytes which were derived from M
LN. (C) 1999 Elsevier Science B.V. All rights reserved.