BACKGROUND: It was assumed that T γδ lymphocytes (T γδ) are involved in the autoimmune destruction of beta cells, presumably as regulatory cells. OBJECTIVES: The aim of this paper was to investigate T γδ cells mean percentage (%) in peripheral blood in patients with type 1 diabetes (T1DM) at the time of diagnosis and after twelve months of observation. MATERIAL AND METHODS: A total of 41 patients (21 boys, 51.2%) with new-onset T1DM were included. Exclusion criteria were: Other autoimmune disease, neoplasm, and inflammation. The control group comprised of 14 healthy (7 boys, 50.0%), normostenic children, with normal glucose metabolism and negative history of autoimmune disease and/or diabetes in family. RESULTS: The mean T γδ % in patients with new-onset T1DM (8.03 ± 3.80) and after 12-months of follow-up (6.13 ± 2.15) was lower than in controls (11.23 ± 6.79), p = 0.042 and p = 0.016, respectively. A depletion of those cells after one year was observed (p = 0.067). Gender did not affect the level of T γδ and subsets. No association between T γδ and age neither in T1DM nor controls was observed. CONCLUSIONS: Our results support the hypotheses that T γδ play a role in T1DM pathogenesis. If so, the decrease of those lymphocytes makes the probands more vulnerable to autoaggression. We report here for the first time the further depletion of T γδ after one year of insulin treatment, which may be due to the exacerbation of beta cell destruction in the course of insulitis.
BACKGROUND: It was assumed that T γδ lymphocytes (T γδ) are involved in the autoimmune destruction of beta cells, presumably as regulatory cells. OBJECTIVES: The aim of this paper was to investigate T γδ cells mean percentage (%) in peripheral blood in patients with type 1 diabetes (T1DM) at the time of diagnosis and after twelve months of observation. MATERIAL AND METHODS: A total of 41 patients (21 boys, 51.2%) with new-onset T1DM were included. Exclusion criteria were: Other autoimmune disease, neoplasm, and inflammation. The control group comprised of 14 healthy (7 boys, 50.0%), normostenic children, with normal glucose metabolism and negative history of autoimmune disease and/or diabetes in family. RESULTS: The mean T γδ % in patients with new-onset T1DM (8.03 ± 3.80) and after 12-months of follow-up (6.13 ± 2.15) was lower than in controls (11.23 ± 6.79), p = 0.042 and p = 0.016, respectively. A depletion of those cells after one year was observed (p = 0.067). Gender did not affect the level of T γδ and subsets. No association between T γδ and age neither in T1DM nor controls was observed. CONCLUSIONS: Our results support the hypotheses that T γδ play a role in T1DM pathogenesis. If so, the decrease of those lymphocytes makes the probands more vulnerable to autoaggression. We report here for the first time the further depletion of T γδ after one year of insulin treatment, which may be due to the exacerbation of beta cell destruction in the course of insulitis.
Entities:
Keywords:
T γδ lymphocytes; immune tolerance; type 1 diabetes
Authors: Felicity Coulter; Amy Parrish; Declan Manning; Beate Kampmann; Joseph Mendy; Mathieu Garand; David M Lewinsohn; Eleanor M Riley; Jayne S Sutherland Journal: Front Immunol Date: 2017-10-11 Impact factor: 7.561