Foxp3+ regulatory T cells in regional lymphs nodes of arthritic TNFRp55-/- mice after Yersinia enterocolitica infection

CARGNELUTTI ETHELINA; DI GENARO MARÍA SILVIA

Buenos Aires

Congreso; First French-Argentine Immunology Congress, LVIII Reunión Científica Anual de la Sociedad Argentina de Inmunología, XIII Jornadas Científicas del Grupo Rioplatense de Citometría de Flujo, 3º Jornadas Argentinas de Inmunodeficiencias Primarias (SAP); 2010

Sociedad Argentina de Inmunología-French Society of Immunology

Foxp3+ regulatory T cells in regional lymph nodes of arthritic TNFRp55-/- mice after Yersinia enterocolitica infection Cargnelutti Ethelina; Di Genaro María Silvia Laboratorio de Inmunopatología, Instituto Multidisciplinario de Investigaciones Biológicas-San Luis(IMIBIO-SL), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad Nacional de San Luis, Argentina. Foxp3+ regulatory T cells (Treg) are CD4+ T cells population that control immune response in several mouse models. There are some works that demonstrated that selectively altering Treg cell distribution in vivo leads to the development of tissue-specific inflammation. We have demonstrated previously that TNFRp55-/- (KO) mice developed more severe and chronic reactive arthritis (ReA), compare with C57BL/6 wild-type (WT) mice, after an oral Yersinia infection. Also, we found that KO mice exhibited significantly differences in IL-10 levels, compared with WT mice, in regional lymph nodes (RLN) to the joint, and in mesenteric lymph nodes (MLN) at different days after infection. In vivo function of Treg cells in ReA remains unclear. The aim of this work was to determine, by flow cytometry analysis, the relative number of Treg cells in RLN and MLN of KO and WT mice, at days 7,14 (arthritis onset) and 21 after an oral Y. enterocolitica O:3 infection, and then, to define the in vivo contribution of Treg cells in our mouse model. A significantly decrease in the relative number of Treg cells was detected in KO mice, at day 14 in RLN, compare with WT mice (3,65%±0,13 and 5,12%±0,46, respectively) (p<0,05). At day 21, KO mice showed higher relative number of Treg cells, compare with WT mice (4,36%± 0,26 and 3,39%±0,29,respectively) (p<0,05). However, the total number of Treg cell was unvaried. In addition, we did not find significantly differences in the relative number of Treg cells in MLN from KO and WT mice. We concluded that in contrast to mucosal site, there is a local correlation between the relative number of Treg cells and the IL-10 levels, found in previous studies. The unvaried Treg cell total number could be the result of an influx of other cells. The decrease relative number of Treg cells at arthritis onset could be responsible of a local unregulated response in this animal model.