In summary, we generated an extensive range of clearly defined and quality controlled gnotobiotic microbiotas in vivo in combination with read-outs for serum IgE levels, intestinal SCFA levels, Treg induction, IgA and IL10 production to identify characteristics of individual or communities of commensal bacterial species with the capacity to suppress the hyper-IgE syndrome observed in germ-free mice. Here, IGHE is linked to hyper-IgE syndrome.