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Mechanisms underlying trypanosome-elicited immunosuppression

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Abstract
T-cell proliferative responses of lymph node cells are profoundly suppressed during experimental infections of mice with Trypanosoma brucei. The active suppression of lymph node T-cell proliferative responses is attributed to the coexistence of at least two unlinked suppressive mechanisms that block different T-cell regulatory steps and operate through different effector mechanisms. The generation of prostaglandin-producing macrophages is entirely responsible for the suppression of IL-2 production whereas the induction of a prostaglandin-independent suppressive mechanism accounts for the suppression of the expression of IL-2 receptors (IL-2R). Both mechanisms are mediated by the cells that co-purify wich macrophages. Despite an impairment at the level of T-cell proliferation, lymph node cells from T brucei infected animals produce substantial amounts of interferon-gamma (IFN-gamma) and this lymphokine participates in the down-regulation of IL-2R expression. T brucei-pulsed macrophage cell lines acquire concomitantly the potential to suppress T-cell proliferative responses and to stimulate CD8+ T-cells to secrete IFN-gamma. The sensibilization of CD8+ T cells by T. brucei-pulsed macrophages might be mediated by TNF-alpha. Collectively, these results indicate that the uptake of T brucei by macrophages, either in vivo or in vitro, results in the generation of suppressive cells that annihilate T-cell proliferative responses. Furthermore, at least two cytokines (i.e. TNF-alpha and IFN-gamma) are released during thse interactions. Besides playing a role in the pathway of T-cell immunosuppression, TNF-alpha and IFN-gamma could also contribute to immunopathological features that occur during trypanosome infections.
Keywords
TRYPANOSOMA-BRUCEI, IMMUNOSUPPRESSION, IL-2, IFN-GAMMA, TNF-ALPHA, INTERLEUKIN-2 RECEPTOR EXPRESSION, BRUCEI-INFECTED MICE, CD8+ T-CELLS, AFRICAN TRYPANOSOMIASIS, PERITONEAL-MACROPHAGES, SUPPRESSION, ACTIVATION, MODULATION, GROWTH, GAMMA

Citation

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Chicago
Darji, A, R Lucas, Stefan Magez, E Torreele, J Palacios, M Sileghem, EB Songa, R Hamers, and P De Baetselier. 1991. “Mechanisms Underlying Trypanosome-elicited Immunosuppression.” Annales De La Societe Belge De Medecine Tropicale 71 (suppl. 1): 27–38.
APA
Darji, A., Lucas, R., Magez, S., Torreele, E., Palacios, J., Sileghem, M., Songa, E., et al. (1991). Mechanisms underlying trypanosome-elicited immunosuppression. ANNALES DE LA SOCIETE BELGE DE MEDECINE TROPICALE, 71(suppl. 1), 27–38. Presented at the Trypanosomiasis seminar.
Vancouver
1.
Darji A, Lucas R, Magez S, Torreele E, Palacios J, Sileghem M, et al. Mechanisms underlying trypanosome-elicited immunosuppression. ANNALES DE LA SOCIETE BELGE DE MEDECINE TROPICALE. 1991;71(suppl. 1):27–38.
MLA
Darji, A et al. “Mechanisms Underlying Trypanosome-elicited Immunosuppression.” ANNALES DE LA SOCIETE BELGE DE MEDECINE TROPICALE 71.suppl. 1 (1991): 27–38. Print.
@article{8572173,
  abstract     = {T-cell proliferative responses of lymph node cells are profoundly suppressed during experimental infections of mice with Trypanosoma brucei. The active suppression of lymph node T-cell proliferative responses is attributed to the coexistence of at least two unlinked suppressive mechanisms that block different T-cell regulatory steps and operate through different effector mechanisms. The generation of prostaglandin-producing macrophages is entirely responsible for the suppression of IL-2 production whereas the induction of a prostaglandin-independent suppressive mechanism accounts for the suppression of the expression of IL-2 receptors (IL-2R). Both mechanisms are mediated by the cells that co-purify wich macrophages. 
Despite an impairment at the level of T-cell proliferation, lymph node cells from T brucei infected animals produce substantial amounts of interferon-gamma (IFN-gamma) and this lymphokine participates in the down-regulation of IL-2R expression. T brucei-pulsed macrophage cell lines acquire concomitantly the potential to suppress T-cell proliferative responses and to stimulate CD8+ T-cells to secrete IFN-gamma. The sensibilization of CD8+ T cells by T. brucei-pulsed macrophages might be mediated by TNF-alpha. Collectively, these results indicate that the uptake of T brucei by macrophages, either in vivo or in vitro, results in the generation of suppressive cells that annihilate T-cell proliferative responses. Furthermore, at least two cytokines (i.e. TNF-alpha and IFN-gamma) are released during thse interactions. Besides playing a role in the pathway of T-cell immunosuppression, TNF-alpha and IFN-gamma could also contribute to immunopathological features that occur during trypanosome infections.},
  author       = {Darji, A and Lucas, R and Magez, Stefan and Torreele, E and Palacios, J and Sileghem, M and Songa, EB and Hamers, R and De Baetselier, P},
  issn         = {0365-6527},
  journal      = {ANNALES DE LA SOCIETE BELGE DE MEDECINE TROPICALE},
  language     = {eng},
  location     = {Antwerp, Belgium},
  number       = {suppl. 1},
  pages        = {27--38},
  title        = {Mechanisms underlying trypanosome-elicited immunosuppression},
  volume       = {71},
  year         = {1991},
}