THE EFFECTS OF CYCLOSPORINE-A AND CYCLOPHOSPHAMIDE ON THE POPULATIONSOF B-CELL AND T-CELL AND VIRUS IN THE HARDERIAN-GLAND OF CHICKENS VACCINATED WITH THE HITCHNER B1 STRAIN OF NEWCASTLE-DISEASE VIRUS

The cellular response to conjunctival vaccination with the Hitchner B1 strain of Newcastle disease virus was studied in the Harderian gland (HG) by immunohistochemistry. Bu-1(+) cells and all subpopulations of T cells, (CD3(+), CD4(+), CD8(+), TCR gamma delta, TCR alpha beta(1), and TCR alpha beta(2)) were in the interstitial tissue between the duc ts and the acini. Plasma cells with cytoplasmic IgM were more disperse d than the other cells and outlined the acini. Bu-1(+) cells and all s ubpopulations of T cells increased at least three-fold after vaccinati on when compared to uninfected birds on the basis of the average cell counts in sections taken at 3, 5, 7, 10, 14, and 20 days after vaccina tion. The most marked increase was in the CD8(+) cells which increased six-fold. Virus replicated for 10 days in cyclophosphamide (Cy) treat ed birds and for 7 days in cyclosporin A (CsA) treated birds compared with 5 days in untreated birds. Cy treatment prevented an antibody res ponse to NDV and reduced Bu-1(+) and IgM cells in the HG by 20-fold. C y treatment resulted in a doubling of the number of T cells in the HG but these T cells may have been transiently disabled because it also c aused a poor response of the lymphocytes in whole blood to the T cell mitogen concanavalin A (ConA). CsA reduced the T cell numbers in the H G and whole-blood responses to ConA by about 4-fold but T cell numbers rebounded to normal resting values after vaccination with NDV. The cl earance time was prolonged either by T cells being less numerous than normal after CsA or being disabled after Cy. T cells, but not B cells, may therefore be essential for virus clearance. CD8(+) cells expanded more than CD4(+) cells after the vaccination of untreated and CsA-tre ated birds indicating that CD8(+) cells may be key players in vaccinal immunity to NDV. (C) 1997 Elsevier Science B.V.