Publikation

CD31 is required on CD4+ T cells to promote T cell survival during Salmonella infection

Wissenschaftlicher Artikel/Review - 06.07.2011

Bereiche
PubMed
DOI

Zitation
Ross E, Buckley C, MacLennan I, Watson S, Khan M, Henderson I, López-Macías C, Gil Cruz C, Hitchcock J, Abhyankar N, Charlesworth J, Hussain K, Marshall J, Bobat S, Flores-Langarica A, Coughlan R, Cunningham A. CD31 is required on CD4+ T cells to promote T cell survival during Salmonella infection. J Immunol 2011; 187:1553-65.
Art
Wissenschaftlicher Artikel/Review (Englisch)
Zeitschrift
J Immunol 2011; 187
Veröffentlichungsdatum
06.07.2011
eISSN (Online)
1550-6606
Seiten
1553-65
Kurzbeschreibung/Zielsetzung

Hematopoietic cells constitutively express CD31/PECAM1, a signaling adhesion receptor associated with controlling responses to inflammatory stimuli. Although expressed on CD4(+) T cells, its function on these cells is unclear. To address this, we have used a model of systemic Salmonella infection that induces high levels of T cell activation and depends on CD4(+) T cells for resolution. Infection of CD31-deficient (CD31KO) mice demonstrates that these mice fail to control infection effectively. During infection, CD31KO mice have diminished numbers of total CD4(+) T cells and IFN-γ-secreting Th1 cells. This is despite a higher proportion of CD31KO CD4(+) T cells exhibiting an activated phenotype and an undiminished capacity to prime normally and polarize to Th1. Reduced numbers of T cells reflected the increased propensity of naive and activated CD31KO T cells to undergo apoptosis postinfection compared with wild-type T cells. Using adoptive transfer experiments, we show that loss of CD31 on CD4(+) T cells alone is sufficient to account for the defective CD31KO T cell accumulation. These data are consistent with CD31 helping to control T cell activation, because in its absence, T cells have a greater propensity to become activated, resulting in increased susceptibility to become apoptotic. The impact of CD31 loss on T cell homeostasis becomes most pronounced during severe, inflammatory, and immunological stresses such as those caused by systemic Salmonella infection. This identifies a novel role for CD31 in regulating CD4 T cell homeostasis.