Stimulated cord blood lymphocytes have a low percentage of Th1 and Th2 cytokine secreting T cells although their activation is similar to adult controls

Similar Potential to Become Activated and Proliferate but Differential Kinetics and Profiles of Cytokine Production of Umbilical Cord Blood T Cells and Adult Blood Naive and Memory T Cells

“…Other studies have investigated the possible differences in cytokine secretion between UCB T cells and AB T cells after polyclonal activation by phytohemagglutinin (PHA), concavalin A, or phorbol myristate acetate (PMA) in combination with ionomycine [17][18][19][20][21][22]. However, the intracellular signalling pathways, and as a consequence also the cytokine responses after activation by these stimuli may significantly differ from the responses after antigen-mediated stimulation [23].…”

Constant IFNγ mRNA to protein ratios in cord and adult blood T cells suggests regulation of IFNγ expression in cord blood T cells occurs at the transcriptional level

“…It has also been suggested that UCB T lymphocytes have an intrinsic defect, the nature of which is unclear, for producing Th1 specific cytokines, and preferentially favour Th2 responses [12,13]. Previous findings from our laboratory have described that upon stimulation with the high concentrations of PMA and ionomycin both CD4 + and CD8 + UCB T lymphocytes expressed mature levels of the activation marker CD69 but did not produce Th1 cytokine such as IFNγ[14]. Therefore, activation of UCB T cells per se does not appear to be blocked, but rather production of Th1 cytokines, like IFNγ, is hindered.…”

Correlation of human decidual and cord blood mononuclear cell cytokine production

“…How the cytokine milieu prior to birth may affect fetal immune development and differentiation is not known. Prescott et al [6] have described universal skewing of the newborn immune response toward a Th2 phenotype, although this is not a consistent finding; other studies suggest a more global reduction in immune function at birth [7][8][9]. It is possible that the cytokine milieu at the maternal-fetal interface may play a role in affecting cytokine expression in the newborn.…”