Santopaolo, Marianna
(2017)
Inflammation in chronic degenerative disorders:
A novel CD3+CD56+ subset that regulates CD8+ T cell effector function.
[Tesi di dottorato]
| 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: |
| Autore | Email |
|---|
| Santopaolo, Marianna | SANTOPAOLOMARIANNA@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: |
| nome | email |
|---|
| Avvedimento, Vittorio Enrico | vittorioenrico.avvedimento@unina.it |
|
| Tutor: |
| nome | email |
|---|
| 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 |
[error in script]
[error in script]
| 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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