CD4(+)TGFβ(+) cells infiltrated the bursa of Fabricius following IBDV infection, and correlated with a delayed viral clearance, but did not correlate with disease severity, or immunosuppression

INTRODUCTION: Infectious Bursal Disease Virus (IBDV) causes immunosuppression in chickens. While B-cell destruction is the main cause of humoral immunosuppression, bursal T cells from IBDV-infected birds have been reported to inhibit the mitogenic response of splenocytes, indicating that some T cell subsets in the infected bursa have immunomodulatory activities. CD4(+)CD25(+)TGFβ(+) cells have been recently described in chickens that have immunoregulatory properties and play a role in the pathogenesis of Marek’s Disease Virus. METHODS: To evaluate if CD4(+)CD25(+)TGFβ(+) cells infiltrated the bursa of Fabricius (BF) following IBDV infection, and influenced the outcome of infection, birds were inoculated at either 2 days or 2 weeks of age with vaccine strain (228E), classic field strain (F52/70), or PBS (mock), and bursal cell populations were quantified by flow cytometry. RESULTS: Both 228E and F52/70 led to atrophy of the BF, a significant reduction of Bu1(+)-B cells, and a significant increase in CD4(+) and CD8α(+) T cells in the BF, but only F52/70 caused suppression of immune responses to a test antigen in younger birds, and clinical signs in older birds. Virus was cleared from the BF more rapidly in younger birds than older birds. An infiltration of CD4(+)CD25(+)T cells into the BF, and elevated expression of bursal TGFβ-1(+) mRNA was observed at all time points following infection, irrespective of the strain or age of the birds, but CD4(+)TGFβ(+)cells and CD4(+)CD25(+)TGFβ(+) cells only appeared in the BF at 28 dpi in younger birds. In older birds, CD4(+)TGFβ(+) cells and CD4(+)CD25(+)TGFβ(+) cells were present at earlier time points, from 7dpi following 228E infection, and from 14 and 28 dpi following F52/70 infection, respectively. DISCUSSION: Our data suggest that an earlier infiltration of CD4(+)TGFβ(+) cells into the BF correlated with a delayed clearance of virus. However, the influx of CD4(+)TGFβ(+) cells and CD4(+)CD25(+)TGFβ(+) into the BF did not correlate with increased pathogenicity, or immunosuppression.