Prevalence of intracellular galectin-1-expressing lymphocytes in umbilical cord blood in comparison with adult peripheral blood.

Abstract

Umbilical cord blood (UCB) is a promising alternative for the treatment of hematological malignancies. The lower immune reactivity of UCB lymphocytes is a well-known phenomenon; however immune tolerance mechanisms are not fully elucidated. Galectin-1 has strong immunosuppressive properties and plays a key role in the regulation of immune reactivity. We aimed to determine the properties of intracellular galectin-1-producing cells within CD3, CD4, CD8, regulatory T and NK cells in UCB compared to adult peripheral blood (APB). We took peripheral blood samples from 22 healthy adults and cord blood samples from 19 healthy, term neonates. Intracellular galectin-1 expression was determined by flow cytometry in the above subsets. Furthermore, we assessed the prevalence of naive and memory T cells that play a role in the regulation of immune reactivity. We also performed functional analyses to assess the effect of exogenous galectin-1 on the rate of proliferation of T lymphocytes isolated from APB and UCB. The prevalence of intracellular galectin-1-expressing CD3, CD4, CD8, Treg and NK lymphocytes was lower in UCB than in ABP. However, their capability to produce galectin-1 reaches the level seen in adults. The prevalence of naive cells was higher, whereas that of central and effector memory T cells was lower in UCB compared with APB. Lower galectin-1-producing cell proportion might be due to the naivity of neonatal lymphocytes, as indicated by the positive correlation detected between the number of CD3 lymphocytes expressing intracellular galectin-1 and the prevalence of memory T cells. The intracellular expression of galectin-1 may be downregulated in neonatal lymphocytes due to the already reduced immune reactivity of UCB. In contrast with previous findings, our results indicate that the administration of exogenous galectin-1 failed to decrease the rate of proliferation in T lymphocytes isolated from either APB or UCB. This suggests that galectin-1-expressing lymphocytes are unlikely to play a major role in mitigating the immune reactivity of UCB.