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Matarese G.,University of Salerno | Colamatteo A.,Unita di NeuroImmunologia | De Rosa V.,Unita di NeuroImmunologia | De Rosa V.,CNR Institute Experimental Endocrinology and Oncology Gaetano Salvatore
Immunology Letters | Year: 2014

The interplay of the immune system with other aspects of physiology is one of the hottest topics of the recent literature. A crucial example is the influence of metabolic cues on immune responses. It is now well accepted that upon activation, T lymphocytes take on a metabolic profile profoundly distinct from that of their quiescent and anergic counterparts; in these sense, T cell metabolism is highly dynamic and has a serious impact on the ability of T cell to grow, activate and differentiate. Specific metabolic pathways provide energy and biosynthetic precursors able to support specific T cell functions, such as effector, regulatory and memory. Here, we review the main signaling pathways that control metabolism and how the metabolic phenotypes of T cell subtypes integrate with their specific function. © 2013 Elsevier B.V.


Mauro C.,Queen Mary, University of London | Rosa V.D.,CNR Institute Experimental Endocrinology and Oncology Gaetano Salvatore | Marelli-Berg F.,Queen Mary, University of London | Solito E.,Queen Mary, University of London
Frontiers in Immunology | Year: 2014

Epidemiological studies reveal an increased incidence of obesity worldwide, which is associated with increased prevalence and severity of cognitive disorders. The blood brain barrier represents the interface between the peripheral circulation and the brain, and plays a fundamental role in the cross-talk between these two compartments. The homeostatic function of the blood-brain barrier is the protection of the brain from peripheral insult/inflammation. Alterations in the function of the blood-brain barrier lead to pathologies of the central nervous system. Recently, metabolic imbalance has been shown to be an important risk factor associated with the decline of blood-brain barrier integrity and function. This has direct etiological consequences to a variety of cerebrovascular and neurodegenerative pathologies with great impact to society. Priority areas for future preclinical research include strategies to improve clinicians? ability to diagnose, prevent, and manage blood-brain barrier abnormalities. In sharp contrast with epidemiological studies and clinical needs, little is known about the mechanisms that link metabolic syndrome to bloodbrain barrier functionality and cognitive disorders. Our view is that immune responses caused by metabolic stress might play a major role in this conundrum. © 2014 Mauro, Derosa, Merelli-berg and Solito.


Galgani M.,CNR Institute Experimental Endocrinology and Oncology Gaetano Salvatore | De Rosa V.,CNR Institute Experimental Endocrinology and Oncology Gaetano Salvatore | Matarese G.,University of Salerno
Molecular Immunology | Year: 2015

During an immune response, T cell differentiation and function are tightly regulated to ensure protection against pathogens and prevent the autoimmune attack versus self-antigens. It is now established that cellular activation is coupled to profound changes in cellular metabolism. Indeed, pathways that control immune cell function and metabolism are intimately related, and different metabolic programs have been shown to control specific T cell fate. This review aims to provide an integrated view of T cell metabolism and of the molecular pathways controlling an appropriate T cell receptor (TCR) engagement. We describe here how different aspects of metabolism can influence T cell functions, focusing on the emerging role of the key metabolic pathways regulating T cell activation and their alterations in different autoimmune conditions. Manipulating these programs or their substrates could provide insights into mechanisms involved in inflammatory/autoimmune conditions, unveiling the potential for developing novel therapeutic approaches to treat these diseases. © 2015 Elsevier Ltd.


La Rocca C.,University of Naples Federico II | La Rocca C.,CNR Institute Experimental Endocrinology and Oncology Gaetano Salvatore | Carbone F.,CNR Institute Experimental Endocrinology and Oncology Gaetano Salvatore | Longobardi S.,Merck Serono SpA | Matarese G.,University of Salerno
Immunology Letters | Year: 2014

Establishment and maintenance of pregnancy represents a challenge for the maternal immune system since it has to defend against pathogens and tolerate paternal alloantigens expressed in fetal tissues. Regulatory T (Treg) cells, a subset of suppressor CD4+ T cells, play a dominant role in the maintenance of immunological self-tolerance by preventing immune and autoimmune responses against self-antigens. Although localized mechanisms contribute to fetal evasion from immune attack, in the last few years it has been observed that Treg cells are essential in promoting fetal survival avoiding the recognition of paternal semi-allogeneic tissues by maternal immune system. Several functional studies have shown that unexplained infertility, miscarriage and pre-clampsia are often associated with deficit in Treg cell number and function while normal pregnancy selectively stimulates the accumulation of maternal forkhead-box-P3+ (FoxP3+) CD4+ Treg cells with fetal specificity. Some papers have been reported that the number of Treg cells persists at elevated levels long after delivery developing an immune regulatory memory against father's antigens, moreover these memory Treg cells rapidly proliferate during subsequent pregnancies, however, on the other hand, there are several evidence suggesting a clear decline of Treg cells number after delivery. Different factors such as cytokines, adipokines, pregnancy hormones and seminal fluid have immunoregulatory activity and influence the success of pregnancy by increasing Treg cell number and activity. The development of strategies capable of modulating immune responses toward fetal antigens through Treg cell manipulation, could have an impact on the induction of tolerance against fetal antigens during immune-mediated recurrent abortion. © 2014 Elsevier B.V.


Procaccini C.,CNR Institute Experimental Endocrinology and Oncology Gaetano Salvatore | Galgani M.,CNR Institute Experimental Endocrinology and Oncology Gaetano Salvatore | De Rosa V.,CNR Institute Experimental Endocrinology and Oncology Gaetano Salvatore | Matarese G.,CNR Institute Experimental Endocrinology and Oncology Gaetano Salvatore | Matarese G.,University of Naples Federico II
Trends in Immunology | Year: 2012

Disorders such as obesity and type 2 diabetes have been linked to immune dysfunction, raising the possibility that metabolic alterations can be induced by or be a consequence of alterations in immunological tolerance. Here, we describe how intracellular metabolic signalling pathways can 'sense' host energy/nutritional status, and in response, modulate regulatory T (Treg) cell function. In particular, we focus on mammalian target of rapamycin (mTOR) signalling, and how stimuli such as nutrients and leptin activate mTOR in an oscillatory manner to determine Treg cell proliferation status. We propose that metabolic changes such as nutritional deprivation or overload could dictate the characteristics of the Treg cell compartment and subsequent downstream immune reactions. © 2011 Elsevier Ltd.

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