At the crossroad of T cells, adipose tissue, and diabetes

Authors

  • Giuseppe Matarese,

    Corresponding author
    1. Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, Napoli, Italy
    • Dipartimento di Medicina, Facoltà di Medicina, Università di Salerno, Baronissi, Salerno, Italy
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  • Claudio Procaccini,

    1. Dipartimento di Medicina, Facoltà di Medicina, Università di Salerno, Baronissi, Salerno, Italy
    2. Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, Napoli, Italy
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  • Veronica De Rosa

    1. Dipartimento di Medicina, Facoltà di Medicina, Università di Salerno, Baronissi, Salerno, Italy
    2. Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, Napoli, Italy
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Correspondence to:

Giuseppe Matarese

Dipartimento di Medicina, Facoltà di Medicina

Università di Salerno, Baronissi Campus

Baronissi 84081, Salerno, Italy

Tel.: +39 081 7464580

Fax: +39 081 7463252

e-mail: gmatarese@unisa.it

Summary

The study of how different intracellular metabolic signaling pathways impact the control of self-immune tolerance and how metabolic dysregulation in overweight, obesity, and diabetes is able to alter self-immune tolerance are topics of intensive investigation. Recent evidence suggests that metabolic and autoimmune diseases, both characterized by chronic inflammation and an altered self-immune tolerance, are more common in affluent countries. The reasons for such phenomena are still not completely understood, but the ‘metabolic pressure’ induced by nutritional overload, typical of more developed countries, seems to play a role. In this context, the discovery of the adipose tissue-derived hormone leptin has shed fundamental insights on how these processes might occur. We believe that there is a strong relationship among leptin, metabolic state, and immunological self-tolerance. We hypothesize that the leptin-induced metabolic pressure sets the basis for an exaggerated immuno-inflammatory response to altered self or non-self, leading to chronic inflammation, metabolic dysregulation, and autoimmunity in subjects with risk factors (i.e. genetic predisposition, environment, sex, infectious agents, etc). Capitalizing on our joint effort and trans-disciplinary expertise in metabolism, self-tolerance, and autoimmune diseases, this review highlights key questions on the basic mechanisms governing immune tolerance in the context of metabolic and autoimmune disease susceptibility.

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