Fig. 1.

In steady-state conditions, microorganisms and their metabolites or food source antigen are the basis of intestinal-related lymphoid tissue (GALT) correct development, through pattern recognition receptor/pathogen-related molecular pattern (PRR–PAMP) recognition start intestinal immunity, promote the dendritic cells, T cells, B cells, innate lymphocyte differentiation or maturation. However, when the intestinal barrier integrity is destroyed and the intestinal mucosal permeability is increased, the intestinal flora and its metabolism can promote caspase-1 precursor activation to caspase-1 through the NLRP 3 inflammasome, and then activate IL-1 β and IL-18, and can also control autophagy through the mTOR pathway. When the intestinal inflammatory cascade expands and the inflammatory products enter the circulatory system, it may cause the occurrence and development of Hashimoto's thyroiditis