While it is supposed to protect us against pathogens (viruses, bacteria, etc.),our immune system can sometimes get out of control. It can then become too sensitive to exogenous constituents and trigger allergies or react against constituents of the self and promote the emergence of autoimmune diseases.

Autoimmune diseases form a group in which we find diseases as different as the dtype 1 diabetes, theremultiple sclerosis, thererheumatoid arthritisor theCrohn's disease. They all correspond to chronic diseases triggered by the body's loss of immunological tolerance to its own constituents.

The vast majority of autoimmune diseases aremultifactorial. With few exceptions, they are believed to be based on a combination of genetic, endogenous, exogenous and/or environmental factors.

The majority of autoimmune diseases are considered to be dependent on agenetic susceptibility, that is to say that their development is favored by one or more genetic particularities (or polymorphisms). Among those incriminated are first of all particular forms ofHLA genes.

Experimental studies or epidemiological data clearly describe aassociation betweenTHEgut microbiota, which is at the interface between the immune system and the environment, and theoccurrence of an autoimmune disease: dysbiosis, which corresponds to a qualitative and quantitative modification of the different species colonizing our digestive system compared to normal conditions, is more frequent in patients than in people without autoimmune diseases.

Exposure to certain compounds or certain pathogens appears to be associated with the risk of autoimmune diseases. Certain environmental pollutants, ultraviolet rays, stress or nutrition are also suspected.

Hence the increasingly demonstrated interest that, in addition to the classic management of autoimmune diseases, an investigation of the state of the intestinal microbiota   and the nutritional state  of the patient are requested.