Publication | Open Access
B cell stimulatory factor-1 enhances the IgE response of lipopolysaccharide-activated B cells.
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1986
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Ige ResponseAdaptive Immune SystemHumoral ResponseImmunologyImmune RegulationImmunologic MechanismInnate ImmunityImmune SystemImmunotherapyB Cell StimulatoryInflammationImmunopathologyCell SignalingMonoclonal AntibodyTh SupernatantsAllergyAutoimmune DiseaseB CellsAutoimmunityHumoral ImmunityCell BiologyLipopolysaccharide-activated B CellsImmunoglobulin EMedicineImmune Cell Activation
Supernatants from certain mouse helper T cell lines can boost IgE production by LPS‑stimulated B cells by at least two orders of magnitude. This IgE‑enhancing activity could not be separated from B cell stimulatory factor‑1 (BSF‑1) during purification. Purified BSF‑1 from the EL‑4 lymphoma line, neutralized by a specific monoclonal antibody, increased IgE, IgG1, and IgG3 production in LPS‑stimulated B cells while leaving IgM, IgG2a, IgG2b, and IgA largely unchanged.
Supernatants from some mouse helper T cell (TH) lines contain an activity that can enhance IgE production by lipopolysaccharide (LPS)-stimulated B cells by at least two orders of magnitude. During purification, this activity could not be resolved from B cell stimulatory factor-1 (BSF-1). Highly purified BSF-1 from a different source, the T lymphoma cell line EL-4, enhanced IgE production to the same extent as TH supernatants, which suggests that BSF-1 is responsible for this increase in IgE production. Monoclonal antibody to BSF-1 totally inhibits the IgE-enhancing activity of a TH supernatant, lending further support to this conclusion. The effects of BSF-1 on LPS-stimulated B cells are specific for IgE and, as previously reported, IgG1 and IgG3, because the levels of IgM, IgG2a, IgG2b, and IgA in the cultures change relatively little when BSF-1 is added.