BACKGROUND: The production of specific IgE, which underlies the allergic response, may be a normal correlate of the immune response to a certain class of antigen (allergens), or could represent a unique response driven by regulatory signals that are absent in non-allergic individuals. If atopic subjects do possess a regulatory environment favoring IgE production, they may display not only allergen-specific IgE, but also higher levels of total IgE and higher frequencies of IgE-producing B lymphocytes. OBJECTIVE: To address the contribution of antibody-producing cell number to the circulating IgE titre in atopic vs non-atopic subjects. METHODS: Frequency determination by limiting dilution of EBV transformants and Poisson distribution analysis. Titres of total and allergen-specific IgM, IgG, and IgE by specific ELISA. RESULTS: In contrast to findings reported by others, the atopic subjects had a significantly higher frequency of IgE-producing B cells than non-atopics (0.79% of total Ig-producing cells, as compared with 0.17% for the control group; P < 0.01), suggesting that one factor contributing to the high plasma IgE titres in atopic subjects is the high frequency of B lymphocytes with the potential to produce IgE. Although only the atopic subjects produced allergen-specific IgE, the frequency of specific IgE-producing B cells was undetectable in both groups. CONCLUSION: Atopic subjects have higher frequencies of IgE-producing B cell precursors than non-atopics. A correlation exists between IgE-producing B cell frequency and levels of circulating IgE.
BACKGROUND: The production of specific IgE, which underlies the allergic response, may be a normal correlate of the immune response to a certain class of antigen (allergens), or could represent a unique response driven by regulatory signals that are absent in non-allergic individuals. If atopic subjects do possess a regulatory environment favoring IgE production, they may display not only allergen-specific IgE, but also higher levels of total IgE and higher frequencies of IgE-producing B lymphocytes. OBJECTIVE: To address the contribution of antibody-producing cell number to the circulating IgE titre in atopic vs non-atopic subjects. METHODS: Frequency determination by limiting dilution of EBV transformants and Poisson distribution analysis. Titres of total and allergen-specific IgM, IgG, and IgE by specific ELISA. RESULTS: In contrast to findings reported by others, the atopic subjects had a significantly higher frequency of IgE-producing B cells than non-atopics (0.79% of total Ig-producing cells, as compared with 0.17% for the control group; P < 0.01), suggesting that one factor contributing to the high plasma IgE titres in atopic subjects is the high frequency of B lymphocytes with the potential to produce IgE. Although only the atopic subjects produced allergen-specific IgE, the frequency of specific IgE-producing B cells was undetectable in both groups. CONCLUSION: Atopic subjects have higher frequencies of IgE-producing B cell precursors than non-atopics. A correlation exists between IgE-producing B cell frequency and levels of circulating IgE.