**1. Introduction**

Immune tolerance is a physiological condition, characterized by the absence of an immune response to a specific antigen and the retention of the ability to develop an immune response to other different antigens. Tolerance to self-components develops both during embryonic development (i.e., central tolerance, which occurs in the primary lymphoid organs, along with the process of lymphocyte differentiation), and after birth (i.e., peripheral tolerance) [1].

Currently, the microbiota is considered an anatomically integrated meta-organ that performs functions through which it interferes with the host's physiology [2]. Thus, microbiota eubiosis is a major parameter of physiological homeostasis.

Human microbiota establishes three types of relationships with the host—symbiotic, commensal, and pathobiontic, respectively [3]. The terms "microbiota" and "microbiome" are equivalent, but not identical. The first refers to the population of microorganisms residing on the mucous membranes of the digestive, urogenital and respiratory tract, as well as on the skin, and the second designates the collective genome of the microbiota, called the metagenome [4]. The community microbiome was evaluated at 3.3 million redundant bacterial genes, about 150 times larger than the human gene complex [5]. The gut microbiota is influenced by various conditions, such as diet, health, mental stress, gender, or exercise, and conversely, it influences all body metabolism, immune reactivity, and behavior [6]. The microbiota contributes to the peripheral tolerance of the immune system toward autoantigens, with the retention of the immune reactivity against all antigens that do not cross-react with the tolerated antigen. Interruption of tolerance initiates an immune response to self-antigens characterized by the production of autoantibodies or autoreactive lymphocytes, which trigger an autoimmune conflict [7]. The purpose of this chapter is to highlight the role of the normal microbiota in the state of immune tolerance and to investigate the correlations of dysbiosis with endocrine AIDS.
