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Diabetes is not a single and homogeneous disease, but a cluster of metabolic diseases characterized by the common feature of hyperglycemia. The pathogenesis of type 1 diabetes (T1D) and type 2 diabetes (T2D) (and all other intermediate forms of diabetes) involves the immune system, in terms of inflammation and autoimmunity. The past decades have seen an increase in all types of diabetes, accompanied by changes in eating habits and consequently a structural evolution of gut microbiota. It is likely that all these events could be related and that gut microbiota alterations might be involved in the immunomodulation of diabetes. Thus, gut microbiota seems to have a direct, even causative role in mediating connections between the environment, food intake, and chronic disease. As many conditions that increase the risk of diabetes modulate gut microbiota composition, it is likely that immune-mediated reactions, induced by alterations in the composition of the microbiota, can act as facilitators for the onset of diabetes in predisposed subjects. In this review, we summarize recent evidence in the field of gut microbiota and the role of the latter in modulating the immune reactions involved in the pathogenesis of diabetes.

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Immunization of Swiss mice with Ehrlich ascites cells which had been exposed in vitro to 42.C for 3 hours is more effective, so far as subsequent tumor transplantation is concerned, than immunization with radiation‐inactivated cells or with cells exposed to 42.5C for 6 hours. These results, which indicate that upon moderate heat treatment there is a definite increase of the immunogencity of these cells, may have some relevance as to the mechanism of the delayed tumor regression which is often clinically observed after hyperthermic perfusion.