A) Key data sources and assumptions used during model fitting, including relative abundance (line plot) and IgA-index (bubble plot) data, each colored by taxon. Model predictions reconstruct ecological dynamics in the gut lumen and the germinal center (GC) reactions. 2Y: 2 years; mSIgA and eSIgA: maternal and endogenous secretory Immunoglobulin A. B) Model dynamics. (i) Breastfeeding and complementary feeding introduce human milk oligosaccharides (HMOs), plant-derived polysaccharides (PDPs), (ii) mSIgA, and (iii) commensal bacteria to the gut lumen as SIgA-bacteria complexes or bacteria alone, alongside with the bacteria seeding the infant’s gut during vaginal birth. The microbiome within the gut lumen (large light blue circle), contains subpopulations of commensals that exist either in an SIgA-bound (white circle, left) or unbound (white circle, right) state, and transition between the two is driven by SIgA coating or degradation. (iv) Bacterial populations modulate the inflammatory tone of the microenvironment of the gut lumen , (v) influencing epithelial cell-mediated communication with the organized gut-associated lymphoid tissue (GALT) inductive sites, and (vi) the antigenic sampling through barrier integrity. (vii) SIgA-bound and unbound antigens sampled by Microfold (M) cells (viii) activate the naïve B cells, and (ix) drive the balance between antigen-specific regulatory vs. helper T cells (indicated by the divide sign). (x) This balance and shape the selection threshold for taxon , (xi) which determines the BCR affinity ranges that lead to different B cell fates: (xii) apoptosis, (xiii) continued circulation, or (xiv) terminal differentiation into IgA-secreting plasma cells. (xv) IgA secreted by the plasma cells regulates the microbiome via (xvi) masking and (xvii) neutralization functions. Alongside the HMOs and PDPs, (xviii) the oxygen concentration (O 2 ) also influences the ecological dynamics based on commensals’ metabolism. C) GC reactions (steps 1–7, materials and methods, corresponding to (x)–(xiv) on the previous panel) . Naïve B cells with a wide BCR affinity distribution migrate from the bone marrow to the GALT inductive sites, and their affinity distribution is combined with that of circulating B-cells. B-cells activate upon encountering bacterial antigens. Based on how close their BCR affinities are to the selection threshold , cells undergo positive selection, receiving adequate T cell help to continue circulating or differentiate to IgA-secreting plasma cells; and if not, become apoptotic. Circulating cells undergo somatic hypermutation (SHM), increasing the standard deviation of their BCR affinity distribution, continuing the cycle.