The Sweet Kiss Breaching Immunological Self-Tolerance

Mario Galgani; Giuseppe Matarese

doi:10.1016/j.molmed.2019.08.003

The Sweet Kiss Breaching Immunological Self-Tolerance

Trends Mol Med. 2019 Oct;25(10):819-820. doi: 10.1016/j.molmed.2019.08.003. Epub 2019 Aug 23.

Authors

Mario Galgani¹, Giuseppe Matarese²

Affiliations

¹ Istituto per l'Endocrinologia e l'Oncologia Sperimentale del Consiglio Nazionale delle Ricerche (IEOS-CNR), 80131 Napoli, Italy.
² Istituto per l'Endocrinologia e l'Oncologia Sperimentale del Consiglio Nazionale delle Ricerche (IEOS-CNR), 80131 Napoli, Italy; Treg Cell Lab, Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università di Napoli Federico II, 80131 Napoli, Italy. Electronic address: giuseppe.matarese@unina.it.

PMID: 31451384
DOI: 10.1016/j.molmed.2019.08.003

Abstract

Metabolic alterations leading to overactivation of nutrient-energy-sensing pathways have been linked to altered immunological self-tolerance. Now, Zhang and colleagues (Immunity, 2019) have identified a key role for high glucose consumption in exacerbating autoimmunity in mice via induction of T helper (Th)17 cells. This reveals a novel mechanism underlying effects of diet during autoimmunity development with major translational implications.

MeSH terms

Animals
Autoimmunity
Cell Count
Colitis / etiology
Colitis / genetics
Colitis / immunology*
Glucose / adverse effects*
Glucose / immunology
Humans
Immune Tolerance*
Mice
Mice, Knockout
Receptor, Transforming Growth Factor-beta Type II / genetics
Receptor, Transforming Growth Factor-beta Type II / immunology
T-Lymphocytes, Regulatory / cytology
T-Lymphocytes, Regulatory / immunology
Th1 Cells / cytology
Th1 Cells / immunology
Th17 Cells / cytology
Th17 Cells / immunology

Substances

Receptor, Transforming Growth Factor-beta Type II
Tgfbr2 protein, mouse
Glucose