Abstract
Human immunodeficiency virus (HIV) infection is characterized by dysfunctional B cell responses. Here we show that chronic simian immunodeficiency virus (SIV) infection is characterized by an expansion of either lymph node germinal center (GC) B cells that co‐express Bcl6, Ki‐67 and IL‐21R and correlate with expanded T follicular helper (Tfh) cells or B cells that lack Bcl6, Ki‐67 and IL‐21R but express high levels of anti‐apoptotic Bcl2 that negatively correlate with Tfh cells. The lack of Tfh cells likely contributes to persistence of dysfunctional non‐proliferating B cells during chronic infection. These findings have implications for protective immunity in HIV‐infected individuals who harbour low frequencies of Tfh cells.
Highlights
B cell dysfunction has been well documented during human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) infections and is characterized by hypergammaglobulinemia or B cell exhaustion.[1]
Dysfunctional responses is thought to be driven by an expansion of T follicular helper (Tfh) cells that likely contribute to hyper‐reactive germinal center (GC) reactions characterized by an expansion of GC B cells that express Bcl[6] and hypergammaglobulinemia.[1,3,4,14,15,16]
We observed similar contrasting phenotypes in chronically infected rhesus macaques with significantly higher frequencies of Bcl6+IgG+ GC B cells in SIV+Bcl6hi animals that positively correlated with Tfh cells, whereas the SIV+Bcl6lo group of animals had little or no Bcl[6] expression but had significantly higher levels of Bcl[2] expression
Summary
B cell dysfunction has been well documented during human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) infections and is characterized by hypergammaglobulinemia or B cell exhaustion.[1] Numerous studies have implicated a role for expanded T follicular helper (Tfh) cells in driving the expansion of B cells in the germinal centers.[2,3,4] On the other hand, lack of help from Tfh cells has been reported to impair B cell immune responses during HIV infection.[5]. Given the anti‐apoptotic nature of Bcl[2], it likely contributes to the expansion and persistence of dysfunctional B cells that display a hypo‐proliferative and IL‐21R− phenotype. These finding provide additional insights into B cell dysfunction observed during chronic HIV infection.
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