During infection, the release of damage-associated molecular patterns, so-called 
"alarmins," orchestrates the immune response. The alarmin IL-33 plays a role in 
a wide range of pathologies. Upon release, IL-33 signals through its receptor 
ST2, which reportedly is expressed only on CD4(+) T cells of the Th2 and 
regulatory subsets. Here we show that Th1 effector cells also express ST2 upon 
differentiation in vitro and in vivo during lymphocytic choriomeningitis virus 
(LCMV) infection. The expression of ST2 on Th1 cells was transient, in contrast 
to constitutive ST2 expression on Th2 cells, and marked highly activated 
effector cells. ST2 expression on virus-specific Th1 cells depended on the 
Th1-associated transcription factors T-bet and STAT4. ST2 deficiency resulted in 
a T-cell-intrinsic impairment of LCMV-specific Th1 effector responses in both 
mixed bone marrow-chimeric mice and adoptive cell transfer experiments. 
ST2-deficient virus-specific CD4(+) T cells showed impaired expansion, Th1 
effector differentiation, and antiviral cytokine production. Consequently, these 
cells mediated little virus-induced immunopathology. Thus, IL-33 acts as a 
critical and direct cofactor to drive antiviral Th1 effector cell activation, 
with implications for vaccination strategies and immunotherapeutic approaches.