Neonatal (cord blood) T cells can competently raise type 1 and 2 immune responses upon polyclonal activation.
In the neonate, cellular immunity has generally been hypothesized as being incompetent. Accumulating evidence from several recent studies, together with our present report, contradicts this hypothesis. T-helper cell and T cytotoxic type 1 and 2 (Th1/Th2 and Tc1/Tc2, respectively) cytokine responses to polyclonal T cell receptor (TCR) activation were assessed in medium-term cultures of human cord blood T cells using intracellular cytokine staining, which could measure the frequencies of cytokine-producing cells. In this study, we examined the responses of cord blood CD4(+) and CD8(+) T cells in regard to the production of interferon (IFN)-gamma and interleukin (IL)-4 and compared the responses with those obtained from T cells of healthy adults. We found that the responses in cord blood T cells activated with TCR stimulation were comparable to those of their adult counterparts. Moreover, the Th/Tc cells that developed in cord blood were as competent as adult cells for both IFN-gamma and IL-4 secretion. In addition, IL-12 production, which is critical for both Th1 and Tc1 responses, was equally comparable in the two groups. The production of two major cross-regulatory cytokines, tumor necrosis factor-alpha and IL-10, was similarly comparable and not significantly different between the two groups. Taken together, these results indicate that, though naive, the neonatal T cell is competent to respond to TCR-mediated stimulation and to produce both type 1 and type 2 cytokines.
Chipeta
J
J
Department of Pediatrics, Department of Clinical Immunology, Mie University School of Medicine, 2-174 Edobashi, Tsu, Mie, 514-8507, Japan.
Komada
Y
Y
Zhang
X L
XL
Azuma
E
E
Yamamoto
H
H
Sakurai
M
M
D000328:Adult; D002478:Cells, Cultured; D005312:Fetal Blood / Q000166:cytology / Q000276:immunology*; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis; D016753:Interleukin-10 / Q000096:biosynthesis; D018664:Interleukin-12 / Q000096:biosynthesis; D007376:Interleukin-2 / Q000096:biosynthesis; D015847:Interleukin-4 / Q000096:biosynthesis; D017493:Leukocyte Common Antigens / Q000276:immunology; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology; D008213:Lymphocyte Activation / Q000187:drug effects / Q000276:immunology*; D016853:Muromonab-CD3 / Q000008:administration & dosage / Q000276:immunology; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D015375:Receptors, Interleukin-2 / Q000096:biosynthesis; D013602:T-Lymphocytes, Cytotoxic / Q000166:cytology / Q000276:immunology*; D018417:Th1 Cells / Q000166:cytology / Q000276:immunology*; D018418:Th2 Cells / Q000166:cytology / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D007376:Interleukin-2; D016853:Muromonab-CD3; D015375:Receptors, Interleukin-2; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D018664:Interleukin-12; D015847:Interleukin-4; D007371:Interferon-gamma; D017493:Leukocyte Common Antigens; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1