Santopaolo, Marianna (2017) Inflammation in chronic degenerative disorders: A novel CD3+CD56+ subset that regulates CD8+ T cell effector function. [Tesi di dottorato]

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Tipologia del documento: Tesi di dottorato
Lingua: English
Titolo: Inflammation in chronic degenerative disorders: A novel CD3+CD56+ subset that regulates CD8+ T cell effector function.
Autori:
AutoreEmail
Santopaolo, MariannaSANTOPAOLOMARIANNA@GMAIL.COM
Data: 6 Aprile 2017
Numero di pagine: 51
Istituzione: Università degli Studi di Napoli Federico II
Dipartimento: Medicina Molecolare e Biotecnologie Mediche
Dottorato: Medicina molecolare e biotecnologie mediche
Ciclo di dottorato: 29
Coordinatore del Corso di dottorato:
nomeemail
Avvedimento, Vittorio Enricovittorioenrico.avvedimento@unina.it
Tutor:
nomeemail
Tramontano, Donatella[non definito]
Data: 6 Aprile 2017
Numero di pagine: 51
Parole chiave: T1D, CD3+CD56+
Settori scientifico-disciplinari del MIUR: Area 06 - Scienze mediche > MED/04 - Patologia generale
Depositato il: 03 Mag 2017 08:48
Ultima modifica: 13 Mar 2018 11:27
URI: http://www.fedoa.unina.it/id/eprint/11557
DOI: 10.6093/UNINA/FEDOA/11557

Abstract

It has been reported that a growing and heterogeneous group of regulatory cell modulate immune response. In particular, regulation of CD8+ T lymphocyte effector functions is critical for tissue homeostasis and immune tolerance control. Here, we report that the co-expression of CD3 and CD56 molecules identify a novel human regulatory T cell population exerting suppressive activity on proliferation, cytotoxicity and IFN- production of TCR-activated human CD8+ T lymphocytes. Regulatory functions of human circulating CD3+CD56+ T lymphocytes require cell-to-cell contact and are exerted in both autologous and allogeneic conditions. Of note, CD3+CD56+ T cells are reduced and functionally impaired in children affected by Type 1 Diabetes (T1D), at disease onset. Conversely the frequency of this cell subset is increased in patients with prostate cancer. Taken together, our findings reveal that freshly isolated human CD3+CD56+ cells specifically control activation of human CD8+ T lymphocytes. Perturbation of number and function of this cell subset may account for the deranged functions of CD8+ T lymphocytes observed in autoimmune conditions, including T1D. Thus, therapeutic manipulation of CD3+CD56+ cells may represent an innovative approach to restore immune function in T1D.

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