| First Author | Hamid MA | Year | 2018 |
| Journal | Eur J Immunol | Volume | 48 |
| Issue | 7 | Pages | 1153-1163 |
| PubMed ID | 29569714 | Mgi Jnum | J:265053 |
| Mgi Id | MGI:6188666 | Doi | 10.1002/eji.201747463 |
| Citation | Hamid MA, et al. (2018) Unexpected involvement of IL-13 signalling via a STAT6 independent mechanism during murine IgG2a development following viral vaccination. Eur J Immunol 48(7):1153-1163 |
| abstractText | In this study, recombinant pox viral vaccination was shown to induce highly elevated IgG2a and low IgG1 antibody expression in mice lacking IL-4 or STAT6, whilst IL-13(-/-) mice exhibited elevated IgG1, but very low IgG2a. These findings revealed that IL-13 and IL-4 differentially regulated antibody development. To understand this further, when STAT6(-/-) mice were given a vaccine co-expressing IL-13Ralpha2 that temporarily sequestered IL-13, significantly reduced IgG2a expression, was detected. These findings for the first time demonstrated that IL-13 regulated IgG2a differentiation utilising an alternative IL-13R signalling pathway independent of STAT6 (IL-13Ralpha2 pathway). This was further corroborated by the (i) elevated IL-13Ralpha2 expression detected on STAT6(-/-) lung MHCII(+) CD11c(+) cells 24 h post IL-13 inhibitor vaccination and ii) significant up-regulation of IL-13Ralpha2 expression on spleen and lung derived MHCII(+) CD11c(+) following inhibition of STAT6 signalling in vitro, or vaccination with IL-4R/STAT6 antagonist in vivo. When T follicular helper (Tfh) cells which regulate antibody differentiation were assessed post vaccination, although no difference in IL-4 expression was observed, greatly reduced IFN-gamma expression was detected in IL-13(-/-) and STAT6(-/-) mice compared to wild-type. These findings support the notion that the balance of IL-13 level at the vaccination site can differentially regulate T and B-cell immune outcomes. |
