Open AccessSignalling via CD28 of human naive neonatal T lymphocytes
Author(s) -
HASSAN J.,
O'NEILL S.,
O'NEILL L. A. J.,
PATTISON U.,
REEN D. J.
Publication year - 1995
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1995.tb06655.x
Subject(s) - cd28 , immunology , immune system , t cell , antigen , secretion , t lymphocyte , biology , interleukin 2 , endocrinology , medicine
SUMMARY Accessory molecules play a crucial role in the development of the T cell response to antigenic challenge. We have examined the role of CD28 in modulating the‘naive’ neonatal T cell response to anti‐CD2‐mediated activation. To compare the role of CD28, neonatal and adult T cells were stimulated with a pair of mitogenic anti‐CD2 antibodies in the presence or absence or anti‐CD28 MoAb. With anti‐CD2 alone, neonatal T cells proliferated slightly but produced no detectable IL‐2, whereas adult T cells proliferated vigorously, with significant IL‐2 production. Costimulation with anti‐CD28 MoAb greatly enhanced the proliferative response of neonatal T cells to levels equivalent to those of adult T cells, whereas adult T cells showed only slight increases. Although IL‐2 secretion was increased in the presence of anti‐CD28 MoAb. neonatal T cell IL‐2 production remained lower than in adults. In contrast, enhancement of IL‐2 mRNA expression in neonates was similar to adult levels. Anti‐CD28 MoAb costimulation increased NFkB levels in neonates, albeit to levels lower than that of adults. The cellular mechanism governing the diminished proliferative response of neonatal T lymphocytes to anti‐CD2 may therefore be due to decreased NFkB induction, reduced IL‐2 mRNA expression and deficient IL‐2 production. Although anti‐CD28 MoAb costimulation enhances all of the above signals, NFkB and IL‐2 levels remain lower than in adults, suggesting the need for further activation requirements in the neonate.