Ligation of Surface Ig by Gut-Derived Antigen Positively Selects Chicken Bursal and Peripheral B Cells

Abstract

In many mammals and birds, B cell lymphopoiesis takes place in GALT, such as the avian bursa of Fabricius. Although BCR expression is sufficient for bursal colonization, the role of BCR ligation in the later stages of bursal B cell lymphopoiesis remains elusive. To address this directly, we introduced a surface Ig–related construct with defined Ag specificity containing the Ag-binding portion of a lamprey variable lymphocyte receptor specific for PE fused to a truncated chicken μ-chain (VLRPETμ) into developing chick embryos. VLRPETμ expression supports bursal follicle colonization, clonal expansion, and Ig V gene diversification. VLRPETμ-expressing B cells migrate to the periphery in the absence of the Ag starting from day 18 of embryogenesis. VLRPETμ-expressing B cells declined rapidly in the bursa and periphery in the absence of Ag after hatch; however, intrabursal injection of PE prolonged survival of VLRPETμ+ bursal and peripheral B cells. Intrabursal introduction of Ag increased emigration of short-lived LT2+ B cells. Peripheral VLRPETμ+ B cells were maintained following intrabursal PE application and contained both short-lived LT2+ and long-lived LT2− B cells. In the chicken bursa, the later stages of B cell development occur in the presence of gut-derived Ag; therefore, we conclude that Ag-mediated ligation of BCR in bursal B cells acts to positively select bursal B cells into both short-lived and long-lived peripheral B cell populations.

Cas9-expressing chickens and pigs as resources for genome editing in livestock

“…In Ovo Functionality of SpCas9 in Chicken Bursal B Cells. Transduction of embryonic B cells was carried out using the RCAS retroviral gene transfer system as previously described (35,(59)(60)(61) (Fig. 3B).…”

Necrotic enteritis in chickens: a review of pathogenesis, immune responses and prevention, focusing on probiotics and vaccination

“…The mechanism for B-cell activation is not well defined in chickens. B-cell activation and antibody production is mediated by a combination of cytokines and cognate antigen (Davani et al, 2014). Infection with CP leads to a significant increase in intestinal IL-4 and IL-10 transcripts (Collier et al, 2008), key cytokines involved in B-cell activation.…”

“…In addition, CP infection leads to induction of transforming growth factor (TGF)-β (Fasina and Lillehoj, 2019) and IL-10 (Yitbarek et al, 2012) cytokine transcripts in the small intestine, traditionally associated with inducing an immunosuppressive milieu. In combination with specific cognate antigens, these cytokines (IL-10, TGF-β, IL-4) can induce antigen-specific B-cell differentiation (Davani et al, 2014). While these mechanisms have not been fully explored in CP-infected chickens, detection of antigen-specific IgY antibodies in vaccinated breeder hens demonstrates class switching (IgM to IgY antibody isotype) as well as the presence of plasma B cells (Keyburn et al, 2013a).…”

Identification, tissue characterization, and innate immune role of Angiogenin-4 expression in young broiler chickens

“…At hatch, more than 90% of bursal cells are IgM + B cells and the growth rate of this organ slows thereafter, with a high proportion of cells dying by apoptosis ( Reynaud et al., 1987 , Lassila, 1989 , Motyka and Reynolds, 1991 ). Only IgM-expressing bursal B cells migrate to the secondary lymphoid organs, including the gut-associated lymphoid tissue (GALT), in the absence of intrabursal antigen from day 18 of embryogenesis until sexual maturity ( Davani et al., 2014 , Ko et al., 2018 ). This may explain the increased chAng4 expression level in bursa on day 1, rather than in the GIT, when compared to day 11 and 22.…”