title: Mesenteric lymph node T cells but not splenic T cells maintain their proliferative response to concanavalin-A following peroral infection with Toxoplasma gondii.
abstract: The suppression of T cell responsiveness which occurs after infection with Toxoplasma gondii in mice has been widely studied using spleen cells. Because the natural route of infection with T. gondii is the peroral route, we examined the proliferative responses of mesenteric lymph node (MLN) cells, in addition to spleen cells, to Concanavalin-A (Con-A) in mice perorally infected with T. gondii. Proliferative responses of spleen cells were significantly suppressed seven and ten days after infection when compared with spleen cells from uninfected mice (62% and 91% reduction, respectively). In contrast, proliferative responses of MLN cells from these infected mice did not differ from those of normal MLN cells. Since IFN-gamma-induced reactive nitrogen intermediate (RNI) production has been reported to play a major role in suppression of proliferative responses in spleen cells of infected mice, we compared production of IFN-gamma and RNI by spleen and MLN cells following infection. MLN cells produced as much IFN-gamma as did spleen cells, but produced 70% less nitrite (as a measure of RNI) after Con-A stimulation. Proliferative responses of MLN cells were suppressed when co-cultured with spleen cells from infected mice, and addition of an inhibitor of RNI to these co-culture inhibited this suppression, suggesting that reduced RNI production by MLN cells contributes to their maintenance of higher proliferative responses. These results demonstrated a clear difference in activity of T cells in the MLN and spleen during the acute stage of the infection.
authors.affiliation: Department of Immunology and Infectious Diseases, Palo Alto Medical Foundation, California 94301, USA.
authors.forename: L E
authors.initials: LE
authors.lastname: Neyer
authors.forename: H
authors.initials: H
authors.lastname: Kang
authors.forename: J S
authors.initials: JS
authors.lastname: Remington
authors.forename: Y
authors.initials: Y
authors.lastname: Suzuki
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000378:metabolism; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D018920:Coculture Techniques; D003208:Concanavalin A / Q000494:pharmacology*; D005260:Female; D007371:Interferon-gamma / Q000276:immunology / Q000378:metabolism; D007376:Interleukin-2 / Q000378:metabolism; D008198:Lymph Nodes / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism / Q000469:parasitology; D016177:Macrophage-1 Antigen / Q000378:metabolism; D008643:Mesentery; D051379:Mice; D008807:Mice, Inbred BALB C; D009573:Nitrites / Q000378:metabolism; D013154:Spleen / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism / Q000469:parasitology; D013601:T-Lymphocytes / Q000166:cytology* / Q000187:drug effects* / Q000378:metabolism / Q000469:parasitology; D014122:Toxoplasma / Q000276:immunology; D014124:Toxoplasmosis, Animal / Q000276:immunology* / Q000378:metabolism; D019323:omega-N-Methylarginine / Q000494:pharmacology