Recombinant interleukin (IL) 2‐induced human B cell differentiation is mediated by autocrine IL6

Publisher Website
Google Scholar
Abstract
The molecular mechanism of the interleukin (IL) 2‐induced differentiation of human B cells has been investigated. The experimental results show that Staphylococcus aureus Cowan strain I (SAC) activation alone induces IL 6 secretion from B cells. When B cells were activated by SAC, there was an increased transcription of the IL 6 mRNA. It reached the peak level by 6 h and rapidly decreased to an undetectable level within 24 h. The IL 6 concentration in the culture supernatants reached the peak at 24–48 h and decreased slightly in the following culture periods. Since IL 2 alone could induce IgG secretion, whether exogenous IL 6 was added or not, and IL 2 did not increase autocrine IL 6 synthesis, it appears that IL 2 induces the IL 6 responsiveness of SAC‐activated B cells to differentiate in the later stage of the culture. The addition of polyclonal anti‐IL 6 antibody inhibited IgG secretion. The antibody still efficiently blocked IgG secretion up to day 5, indicating an important role of autocrine IL 6 in the IL 2‐driven B cell differentiation. However, the saturation dose of anti‐IL 6 antibody inhibited 50%–70% of IgG secretion, suggesting that IL 2‐induced B cell differentiation appears to be mediated by other factors besides IL 6.