The hygiene hypothesis suggests that reduced exposure to infections in Western and developing countries has contributed to the rise in autoimmune and allergic diseases. This hypothesis is supported by epidemiological data showing that migrants from low-incidence countries develop these diseases at higher rates in high-incidence countries. Animal models and some clinical trials support the hypothesis, indicating that infections may protect against immune disorders. Mechanisms include reduced homeostatic factors and immunoregulation, involving regulatory T cells and Toll-like receptor stimulation. Changes in microbiota due to lifestyle changes may also play a role. The hypothesis is further supported by the geographical distribution of these diseases, which mirrors that of infectious diseases. Socio-economic factors and migration studies also support the hypothesis. However, the causal relationship remains unclear. Evidence from animal models and clinical trials suggests that infections or their components may have protective effects against immune disorders. Probiotics and helminth parasites have shown potential in preventing allergic and autoimmune diseases. The role of microbiota in the hygiene hypothesis is increasingly recognized, with changes in gut microbiota potentially contributing to immune disorders. Mechanisms such as Th1-Th2 deviation, antigenic competition, immunoregulation, and non-antigenic ligands are involved. The hypothesis also highlights the importance of gene-environment interactions. While there is evidence supporting the hypothesis, further research is needed to confirm its mechanisms and develop effective therapies.The hygiene hypothesis suggests that reduced exposure to infections in Western and developing countries has contributed to the rise in autoimmune and allergic diseases. This hypothesis is supported by epidemiological data showing that migrants from low-incidence countries develop these diseases at higher rates in high-incidence countries. Animal models and some clinical trials support the hypothesis, indicating that infections may protect against immune disorders. Mechanisms include reduced homeostatic factors and immunoregulation, involving regulatory T cells and Toll-like receptor stimulation. Changes in microbiota due to lifestyle changes may also play a role. The hypothesis is further supported by the geographical distribution of these diseases, which mirrors that of infectious diseases. Socio-economic factors and migration studies also support the hypothesis. However, the causal relationship remains unclear. Evidence from animal models and clinical trials suggests that infections or their components may have protective effects against immune disorders. Probiotics and helminth parasites have shown potential in preventing allergic and autoimmune diseases. The role of microbiota in the hygiene hypothesis is increasingly recognized, with changes in gut microbiota potentially contributing to immune disorders. Mechanisms such as Th1-Th2 deviation, antigenic competition, immunoregulation, and non-antigenic ligands are involved. The hypothesis also highlights the importance of gene-environment interactions. While there is evidence supporting the hypothesis, further research is needed to confirm its mechanisms and develop effective therapies.