Suppression of epithelial proliferation and tumorigenesis by IgA.

Oral IgA suppresses steady-state colonic epithelial proliferation and protects IgA-deficient mice from endogenous colorectal tumors, with effects linked to antibody structure and DMBT1.

• Why it matters: IgA deficiency is common and hard to study in humans, and its role in regulating microbiota-driven epithelial growth and colorectal tumorigenesis is unclear.
• What they did: In genetically and environmentally controlled mice, the authors tested IgA deficiency across cancer models, then used oral IgA treatment, reductionist epithelial cultures, and DMBT1 identification via co-immunoprecipitation mass spectrometry and targeted CRISPR screening.
• The result: IgA reduced proliferation and tumor susceptibility, and IgA-mediated suppression required DMBT1; in IgA-knockout mice, deleting DMBT1’s transmembrane and cytoplasmic signaling parts reversed both proliferation and tumor susceptibility.

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