From the Research
Transforming growth factor-beta (TGF-β) is the primary cytokine responsible for inducing B cells to produce IgA antibodies, which are excellent at preventing pathogen attachment to mucous membranes but poor at fixing complement. This process is critical for mucosal immunity as IgA antibodies are the predominant immunoglobulin found in mucosal secretions, including those in the respiratory, gastrointestinal, and genitourinary tracts. TGF-β works by promoting isotype switching in B cells, specifically directing them to change from producing IgM to producing IgA, as demonstrated in a study published in the European journal of immunology 1. While other cytokines such as IL-5, IL-6, and IL-10 can also influence IgA production, TGF-β plays a central role in this process, often working synergistically with these cytokines to enhance IgA production, as shown in a study published in the European cytokine network 2. The importance of TGF-β in IgA production is further underscored by studies showing that mice lacking TGF-β signaling have significantly reduced IgA levels, highlighting its essential role in mucosal immunity. Some studies have also investigated the effects of other cytokines, such as IL-10, on TGF-β production and IgA secretion, demonstrating that IL-10 can modulate TGF-β production and TGF-β receptor expression in activated human B lymphocytes 2. However, based on the most recent and highest quality evidence, TGF-β is the key cytokine responsible for the observed changes in B cell function, specifically the production of IgA antibodies. Key points to consider include:
- TGF-β promotes isotype switching to IgA in B cells
- IgA antibodies are critical for mucosal immunity
- TGF-β works synergistically with other cytokines to enhance IgA production
- The importance of TGF-β in IgA production is supported by studies in mice lacking TGF-β signaling
- IL-10 can modulate TGF-β production and IgA secretion in human B lymphocytes, as demonstrated in a study published in the European cytokine network 2.