Flow Cytometric Analysis of B Cell and T Cell Subpopulations in Specific-Pathogen-Free Chickens Infected with Infectious Bursal Disease Virus

Abstract

Lymphocytes obtained from the blood, spleen, and bursa of normal chickens and of chickens infected with infectious bursal disease virus (IBDV) were analyzed for phenotypic expression of CT4, CT8, and immunoglobulin cell surface markers. Single-cell suspensions were stained with monoclonal antibodies by an indirect immunofluorescent assay, and percent staining was quantitated by flow cytometry. Although an appreciable decline from control levels in the percentage of lymphocytes expressing IgM was detected in the spleen and bursa of infected chickens, the relative proportions of lymphocytes expressing CT4 and CT8 in peripheral blood and spleen remained unchanged following infection. These results suggest that whereas humoral immune depression by IBDV may be associated with lysis of antibody-producing B cells, cellular immune depression is not associated with a detectable change in the proportion of helper or cytotoxic/suppressor subpopulations of T lymphocytes.

T-Cell suppression by cyclosporin-A enhances infectious bursal disease virus infection in experimentally infected chickens

“…IBDV-infected chickens become deficient in the production of optimum levels of antibodies against diverse antigens (Giambrone et al, 1977;Rodenberg et al, 1994). Although T cells do not serve as targets for IBDV replication, cell-mediated immune responses of virus-exposed chickens are compromised.…”

Interaction of infectious bursal disease virus with the immune system of poultry

“…It has been noted that the relative proportions of the CD4 and CD8 cells did not change in the BF after infection with cvIBDV (Rodenberg et al, 1994), although converse to these results, Williams and Davison (2005) found that CD4 and CD8 cells were obvious at 3 and 5 dpi respectively and remained at higher levels until 14 days. The γδTCR+ Tcell population was not affected in the thymus and showed a slight increase (P< 0.05) only at 5 dpi in BF after vvIBDV (strain UK661) infection (Williams and Davison, 2005).…”

“…Perforin and granzyme-A dependant cytotoxic pathways of the cytotoxic T cell are mainly involved in the clearance of the IBDV from the BF, due to higher expression of these proteins in the CD4 and CD8 and BF cells (Rauf et al, 2011b). CD4 and CD8 cells populations appeared to increase in the BF, decrease in the thymus (particularly in the cortex), and show an increasing trend for CD4 and decreasing CD8, which was observed in the spleen in vvIBDV infected chickens (Carballeda et al, 2014), although results from work by Rodenberg et al (1994) were contradictory. It is not clear whether these higher populations are due to cell migration from the tissues to the periphery or contractions of the resident cells (Rasoli et al, 2015).…”

A B-cell targeting virus disrupts potentially protective genomic methylation patterns in lymphoid tissue by increasing global 5-hydroxmethylcytosine levels

“…IBDV targets cells of the BF where the virus predominantly focuses on infecting actively proliferating and differentiating lymphocytes of the B-cell lineage of the chicken [25]. Reports have documented global genomic changes in methylation patterns, including the novel epigenetic mark 5hmC, during both hallmarks of vertebrate Figure 2 The distribution of 5hmC and 5mC relative to B-cell localisation within the embryonic bursa of Fabricius.…”

“…Avian B-cells are crucial for inducing antibody responses against viral pathogens; in response viruses that infect birds often target B-cells to avoid elimination [22,23]. One such pathogen of veterinary and economic significance is infectious bursal disease virus (IBDV) which infects and subsequently causes cell death of developing B-cells as part of a mechanism to avoid elimination from the host [23][24][25]. Chickens within a commercially produced flock can recover from IBDV infection but remain immunosuppressed due, in part, to a reduced B-cell capacity.…”