Background: High expression of CD26, the ectoenzyme dipeptidylpeptidase IV, among CD8+ T cells has been suggested to be a marker of effective long-term memory T cell formation. We characterised CD26 expression of T cell subsets in patients with type 1-diabetes (T1D), who are at increased risk of persistent viral infections, compared to healthy subjects. Materials and methods: Peripheral blood was obtained from 48 outclinic T1D (mean age 48 ± 13 years, disease duration 26 ± 14 years, HbA1c 8.2 ± 1.3%) and 18 age-gender-matched control subjects (48 ± 15 years, HbA1c 5Æ4 ± 0Æ3%). Immunophenotypic analyses were performed by flow cytometry with a panel of monoclonal antibodies (anti-CD4, anti-CD8, and anti- CD26). Results: No significant difference was seen in percentages or absolute numbers of CD4+CD26+, CD4+CD26–, CD8+CD26+, and CD++CD26– between T1D and control people. The fluorescence intensity of CD26 expression on CD8+ lymphocytes revealed a significant decrease in T1D patients (mean fluorescence intensity 18 ± 7 vs. 23 ± 10, P < 0Æ05), whereas the intensity of CD26 expression of CD4+ cells showed no differences between T1D patients and control subjects. Mean fluorescence of CD8+CD26+ cells was inversely correlated with the absolute number of CD4+CD26– cells (R = 0Æ38, P < 0Æ01). Conclusions: Although the precise role of CD26 in T cells has not yet been identified, it is preferentially expressed in CD45RO+ memory T cells and is upregulated upon T cell activation. The observed low expression of CD26 among CD8+ T cells of T1D patients may suggest either a defect in successfully developed long-term memory CD8+ T cells or in CD8+ T cells activation. However, the negative association with the number of CD4+CD26– T cell does not support a recent activation of peripheral T cells. Future investigations should confirm and elucidate the finding of a restricted subset of CD8+ T cells expressing CD26bright in people with TID.

CD26high CD8+ lymphocytes in type 1 diabetes mellitus

MATTEUCCI, ELENA;GIAMPIETRO, OTTAVIO
2010-01-01

Abstract

Background: High expression of CD26, the ectoenzyme dipeptidylpeptidase IV, among CD8+ T cells has been suggested to be a marker of effective long-term memory T cell formation. We characterised CD26 expression of T cell subsets in patients with type 1-diabetes (T1D), who are at increased risk of persistent viral infections, compared to healthy subjects. Materials and methods: Peripheral blood was obtained from 48 outclinic T1D (mean age 48 ± 13 years, disease duration 26 ± 14 years, HbA1c 8.2 ± 1.3%) and 18 age-gender-matched control subjects (48 ± 15 years, HbA1c 5Æ4 ± 0Æ3%). Immunophenotypic analyses were performed by flow cytometry with a panel of monoclonal antibodies (anti-CD4, anti-CD8, and anti- CD26). Results: No significant difference was seen in percentages or absolute numbers of CD4+CD26+, CD4+CD26–, CD8+CD26+, and CD++CD26– between T1D and control people. The fluorescence intensity of CD26 expression on CD8+ lymphocytes revealed a significant decrease in T1D patients (mean fluorescence intensity 18 ± 7 vs. 23 ± 10, P < 0Æ05), whereas the intensity of CD26 expression of CD4+ cells showed no differences between T1D patients and control subjects. Mean fluorescence of CD8+CD26+ cells was inversely correlated with the absolute number of CD4+CD26– cells (R = 0Æ38, P < 0Æ01). Conclusions: Although the precise role of CD26 in T cells has not yet been identified, it is preferentially expressed in CD45RO+ memory T cells and is upregulated upon T cell activation. The observed low expression of CD26 among CD8+ T cells of T1D patients may suggest either a defect in successfully developed long-term memory CD8+ T cells or in CD8+ T cells activation. However, the negative association with the number of CD4+CD26– T cell does not support a recent activation of peripheral T cells. Future investigations should confirm and elucidate the finding of a restricted subset of CD8+ T cells expressing CD26bright in people with TID.
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11568/138230
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo

Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? 0
social impact