Critical role of OX40/OX40L in ILC2-mediated activation of CD4⁺T cells during respiratory syncytial virus infection in mice.

CD4⁺T cells are crucial cellular source of type 2 cytokines and responsible for RSV-induced asthma-like symptoms and asthma exacerbations. However, the mechanism for regulating the activation of CD4⁺T cells during RSV infection is not clear completely. We show in this study that infection with RSV may induce an expansion and activation of CD4⁺T cells in the lungs of BALB/c mice. RSV-induced CD4⁺T cell expansion and activation seems to depend upon the pulmonary group 2 innate lymphoid cells (ILC2s), since adoptive transfer of lung ILC2s can enhance not only the numbers of CD4⁺T cells but also the cytokine production by CD4⁺T cells. Interestingly, blockade of the contact between ILC2s and CD4⁺T cells, may significantly diminish the CD4⁺T cell expansion and cytokine production, suggesting that membrane molecules may be involved in ILC2-regulated CD4⁺T cell activation. In fact, infection with RSV resulted in an increase in the numbers of OX40⁺CD4⁺T cells as well as OX40L⁺ILC2s in the lungs of mice. Moreover, the mRNA expressions of OX40 and OX40L as well as the levels of OX40 and OX40L proteins in the lung CD4⁺T cells and ILC2s were elevated respectively. When co-culture of CD4⁺T cells with ILC2s in the presence of anti-OX40L antibody, the cytokine productions by CD4⁺T cells were reduced markedly, suggesting that lung ILC2s may regulate RSV-induced CD4⁺T cell expansion and activation perhaps via OX40/OX40L interaction.

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