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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| Item Type: | Tesi di dottorato |
|---|---|
| Resource language: | English |
| Title: | Inflammation in chronic degenerative disorders: A novel CD3+CD56+ subset that regulates CD8+ T cell effector function. |
| Creators: | Creators Email Santopaolo, Marianna SANTOPAOLOMARIANNA@GMAIL.COM |
| Date: | 6 April 2017 |
| Number of Pages: | 51 |
| Institution: | Università degli Studi di Napoli Federico II |
| Department: | 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 UNSPECIFIED |
| Date: | 6 April 2017 |
| Number of Pages: | 51 |
| Keywords: | T1D, CD3+CD56+ |
| Settori scientifico-disciplinari del MIUR: | Area 06 - Scienze mediche > MED/04 - Patologia generale |
| Date Deposited: | 03 May 2017 08:48 |
| Last Modified: | 13 Mar 2018 11:27 |
| URI: | http://www.fedoa.unina.it/id/eprint/11557 |
| DOI: | 10.6093/UNINA/FEDOA/11557 |
Collection description
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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