At the crossroad of T cells, adipose tissue, and diabetes
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 m...
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| Published in | Immunological reviews Vol. 249; no. 1; pp. 116 - 134 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Blackwell Publishing Ltd
01.09.2012
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0105-2896 1600-065X 1600-065X |
| DOI | 10.1111/j.1600-065X.2012.01154.x |
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| Abstract | 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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| AbstractList | 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. 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.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. 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. |
| Author | Procaccini, Claudio Matarese, Giuseppe De Rosa, Veronica |
| Author_xml | – sequence: 1 givenname: Giuseppe surname: Matarese fullname: Matarese, Giuseppe email: gmatarese@unisa.it organization: Dipartimento di Medicina, Facoltà di Medicina, Università di Salerno, Baronissi, Salerno, Italy – sequence: 2 givenname: Claudio surname: Procaccini fullname: Procaccini, Claudio organization: Dipartimento di Medicina, Facoltà di Medicina, Università di Salerno, Baronissi, Salerno, Italy – sequence: 3 givenname: Veronica surname: De Rosa fullname: De Rosa, Veronica organization: Dipartimento di Medicina, Facoltà di Medicina, Università di Salerno, Baronissi, Salerno, Italy |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22889219$$D View this record in MEDLINE/PubMed |
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The study of how different intracellular metabolic signaling pathways impact the control of self‐immune tolerance and how metabolic dysregulation in... The study of how different intracellular metabolic signaling pathways impact the control of self‐immune tolerance and how metabolic dysregulation in... The study of how different intracellular metabolic signaling pathways impact the control of self-immune tolerance and how metabolic dysregulation in... |
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| SubjectTerms | Adipose tissue Adipose Tissue - immunology Adipose Tissue - metabolism Animals Autoimmune diseases Autoimmune Diseases - immunology Body Weight diabetes Diabetes mellitus Diabetes Mellitus - immunology Diabetes Mellitus - metabolism Energy Metabolism Hormones Humans Immune Tolerance Immunological tolerance Inflammation Inflammation - immunology Inflammation - metabolism Joint diseases Leptin Leptin - metabolism Lymphocytes T Metabolism Obesity Pressure Risk factors Self Tolerance Sex Signal Transduction T cells T-Lymphocytes - immunology T-Lymphocytes - metabolism Treg |
| Title | At the crossroad of T cells, adipose tissue, and diabetes |
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