Research Abstract |
Several kinds of cytokines were identified in blood plasma when heparinized whole blood was stimulated directly with various stimuli, such as bacteria, bacterial products, and lectins. Immunohistologic and in situ hybridization studies confirmed that IL-1, IL-6, and EFN-gamma were produced almost exclusively by stimulated monocytes in this whole blood system. IL-6 producing ability of cord blood from neonates with over 1,800 gm of birth weight was comparable to adult controls, while very low birth weight infants born at less than 30 weeks of gestation weighing less than 1,500 gm showed poor ability to produce IL-6. It has been claimed that isoform expression patterns of CD45 antigen family denote mutually exclusive two T cell subsets : "naive" T cells expressing CD45RA^+, RO^- and "memory T cells with CD45RO^-, RO^+ phenotype. Almost all T cells in cord blood expressed naive phenotype. Relative proportions of circulating memory T cells increased with advancing age and reached adult leve
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ls around 12 years of age. By using reverse transcriptase/PCR technology, it was confirmed that CD4^+CD45RO^- naive T cells could not express mRNAs for IL-4, IL-5, and IFN-gamma on stimulation. CD4^+, CD45RO^+ memory T cells had the ability to produce these lymphokines. In addition, CD4^+ naive T cells as well as whole cord CD4^+ T cells exerted no significant help for B cell differentiation, while CD4^+ memory T cells acted as an efficient helper in PWM- stimulated coculture system. In vitro stimulation of CD4^+ naive T cells and whole cord CD4^+ T cells with PHA in the presence of exogenous IL-2 caused phenotypic conversion from CD45RO^- to CD45RO^+. Following phenotype conversion, originally naive CD4^+ T cells acquired some memory T cellーlike function. FACS-purified CD4^+ naive T cells could not respond to a combination of anti-CD2 antigens in the absence of monocytes, whereas CD4^+ memory T cells showed vigorous proliferation. CD4^+ memory T cells, but not CD4^+ naive T cells, could produce IL-6 in response to anti-CD2. Whether IL-6 was produced or not seems to be crucial for anti-CD-2mediated cellular proliferation. Less
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