Vdelta2 T-lymphocyte responses in cord blood samples from Italy and Côte d'Ivoire.

Institute of Human Virology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Immunology (Impact Factor: 3.74). 08/2008; 124(3):380-7. DOI: 10.1111/j.1365-2567.2007.02784.x
Source: PubMed

ABSTRACT Cord blood T lymphocytes are immature and their functional defect partially reflects a suboptimal level of costimulatory signals provided by neonatal antigen-presenting cells. Neonatal Vdelta2 T lymphocytes, a small component of cellular immunity involved in the response against bacteria, protozoa, virus-infected cells and tumours, are also considered to be immature. Cord blood Vdelta2 T lymphocytes are mostly naïve, proliferate poorly and do not produce cytokines in response to the model phosphoantigen isopentenyl pyrophosphate. We cultured cord blood mononuclear cells with the aminobisphosphonate Pamidronate or with live bacille Calmette-Guérin, and showed that both elicit a strong cord blood Vdelta2 T-cell proliferative response, inducing the expression of activation markers and promoting the differentiation from naïve to memory cells. Our results suggest that cord blood Vdelta2 T cells are not inherently unresponsive and can mount strong responses to aminobisphosphonates and mycobacteria. Neonatal Vdelta2 T lymphocytes may be important participants in responses to microbial infections early in life.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Neonates have little immunological memory and a developing immune system, which increases their vulnerability to infectious agents. Recent advances in the understanding of neonatal immunity indicate that both innate and adaptive responses are dependent on precursor frequency of lymphocytes, antigenic dose and mode of exposure. Studies in neonatal mouse models and human umbilical cord blood cells demonstrate the capability of neonatal immune cells to produce immune responses similar to adults in some aspects but not others. This review focuses mainly on the developmental and functional mechanisms of the human neonatal immune system. In particular, the mechanism of innate and adaptive immunity and the role of neutrophils, antigen presenting cells, differences in subclasses of T lymphocytes (Th1, Th2, Tregs) and B cells are discussed. In addition, we have included the recent developments in the neonatal mouse immune system. Understanding neonatal immunity is essential to development of therapeutic vaccines to combat newly emerging infectious agents.
    Expert Review of Clinical Immunology 08/2014; · 3.34 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background. P. falciparum (Pf) placental infection primes the fetal immune system and alters infant immunity. Mechanisms leading to these outcomes are not completely understood. We focused on Vγ2 Vδ2 cells, which are part of the immune response against many pathogens, including Pf. These unconventional lymphocytes respond directly to small, non-peptidic antigens, independent of MHC presentation. We wondered whether placental malaria (PM), which may increase fetal exposure to Pf metabolites, triggers a response by neonatal Vγ2 Vδ2 lymphocytes that can be a marker for the extent of fetal exposure to malarial antigens.Methods. Cord blood mononuclear cells were collected from 15 neonates born to mothers with Pf infection during pregnancy (8 with PM) and 25 unexposed neonates. Vγ2 Vδ2 cell phenotype, repertoire and proliferative responses were compared for Pf -exposed and unexposed newborns.Results. PM-exposed neonates had increased proportions of central memory Vγ2 Vδ2 cells in cord blood, with altered Vγ2 chain repertoire ex vivo and after stimulation.Conclusion. Our results suggest that PM affects phenotype and repertoire of neonatal Vγ2 Vδ2 lymphocytes. PM may lower the capacity for subsequent Vγ2 Vδ2 cell responses and impair natural resistance to infectious diseases or response to pediatric vaccination.
    The Journal of Infectious Diseases 12/2013; · 5.85 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Preterm infants are very susceptible to infections. Immune response mechanisms in this group of patients and factors that influence cord blood mononuclear cell populations remain poorly understood and are considered insufficient. However, competent immune functions of the cord blood mononuclear cells are also described. The aim of this work was to evaluate the T-cell population (CD3(+)) with its subpopulations bearing T-cell receptor (TCR) αβ or TCR γδ in the cord blood of preterm infants born before 32 weeks of gestation by mothers with or without an intrauterine infection. Being a pilot study, it also aimed at feasibility check and assessment of an expected effect size. The cord blood samples of 46 infants age were subjected to direct immunofluorescent staining with monoclonal antibodies and then analyzed by flow cytometry. The percentage of CD3(+) cells in neonates born by mothers with diagnosis of intrauterine infection was significantly lower than in neonates born by mothers without infection (p = 0.005; Mann-Whitney U test). The number of cells did not differ between groups. Infection present in the mother did not have an influence on the TCR αβ or TCR γδ subpopulations. Our study contributes to a better understanding of preterm infants' immune mechanisms, and sets the stage for further investigations.
    Archivum Immunologiae et Therapiae Experimentalis 08/2013; · 2.38 Impact Factor

Full-text (2 Sources)

Available from
Oct 27, 2014