Chapter 3

Regulation of Immunity to Tuberculosis

Susanna Brighenti

Susanna Brighenti

Center for Infectious Medicine (CIM), F59, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden

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Diane J. Ordway

Diane J. Ordway

Mycobacteria Research Laboratories, Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO, 80523

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First published: 01 September 2017

Summary

Homeostasis in the immune system has the essential function to minimize deleterious immune-mediated inflammation caused by commensal microorganisms, immune responses against self and environmental antigens, as well as metabolic inflammatory conditions. Homeostatic regulation is enabled by regulatory T (Treg) cells that mediate immune suppression as a vital mechanism of negative regulation. Treg cells have the capacity to prevent not only potentially damaging autoimmune responses, but also protective immunity, and thus the number of Treg cells is a crucial determinant of the regulatory burden on the immune system. The presence of low numbers of Treg cells can trigger fatal autoimmunity, whereas having high numbers can cause overt immunosuppression. Specifically, this means that the combination of the overall number and specific subsets of regulatory cells maintains the order in the immune system by a process of imposing negative regulation on other cells in the immune system. In this review, we will discuss the role of the distinct regulatory immune cell subsets in the development of tuberculosis (TB).

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