IL-12 produced by antigen-presenting cells induces IL-2-independent proliferation of T helper cell clones.


Journal article


S. Maruo, K. Toyo-oka, M. Oh‐hora, X. Tai, H. Iwata, H. Takenaka, S. Yamada, S. Ono, T. Hamaoka, M. Kobayashi, M. Wysocka, G. Trinchieri, H. Fujiwara
Journal of immunology, 1996

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APA   Click to copy
Maruo, S., Toyo-oka, K., Oh‐hora, M., Tai, X., Iwata, H., Takenaka, H., … Fujiwara, H. (1996). IL-12 produced by antigen-presenting cells induces IL-2-independent proliferation of T helper cell clones. Journal of Immunology.


Chicago/Turabian   Click to copy
Maruo, S., K. Toyo-oka, M. Oh‐hora, X. Tai, H. Iwata, H. Takenaka, S. Yamada, et al. “IL-12 Produced by Antigen-Presenting Cells Induces IL-2-Independent Proliferation of T Helper Cell Clones.” Journal of immunology (1996).


MLA   Click to copy
Maruo, S., et al. “IL-12 Produced by Antigen-Presenting Cells Induces IL-2-Independent Proliferation of T Helper Cell Clones.” Journal of Immunology, 1996.


BibTeX   Click to copy

@article{s1996a,
  title = {IL-12 produced by antigen-presenting cells induces IL-2-independent proliferation of T helper cell clones.},
  year = {1996},
  journal = {Journal of immunology},
  author = {Maruo, S. and Toyo-oka, K. and Oh‐hora, M. and Tai, X. and Iwata, H. and Takenaka, H. and Yamada, S. and Ono, S. and Hamaoka, T. and Kobayashi, M. and Wysocka, M. and Trinchieri, G. and Fujiwara, H.}
}

Abstract

We investigated the role of IL-12 in proliferation of various Th cell clones (class II-alloreactive (4-86 and 4-55) and keyhole limpet hemocyanin + self I-Ek-reactive (9-16)) following stimulation with Ag on APCs. These clones proliferated in response to stimulation with rIL-2, rIL-12, or Ag/APC. The proliferation induced by Ag/APC stimulation was not affected by anti-IL-2 Ab but was markedly inhibited by anti-IL-12 Abs. Consistent with this finding was the absence of detectable IL-2 activity in culture supernatants 12 to 48 h after Ag/APC stimulation, and the detection of significant levels of IL-12 in an Ab-capture bioassay. IL-12 was produced within 12 h after Ag/APC stimulation, reaching a peak after 18 to 24 h. The production of IL-12 in cultures of Th clones and APC contrasted with the production of IL-2 but not IL-12 upon allostimulation of primary T cells and the inhibition of their proliferation exclusively by anti-IL-2 Abs. Analysis of the expression of IL-12-binding sites on Th cells revealed low levels of IL-12 receptors in resting Th clones but high IL-12R levels 2 to 3 days after Ag/APC stimulation, declining gradually thereafter. The changes in IL-12R expression levels correlated closely with the IL-12 responsiveness of Th populations at various times after Ag/APC stimulation; Th populations obtained 3 and 10 days after Ag/APC stimulation exhibited very high and weak or marginal responsiveness to rIL-12, respectively, whereas the responses to rIL-2 were comparable in both Th populations. These results indicate that the Ag/APC-stimulated proliferation of terminally differentiated Th clones, in contrast to naive T cells, depends on the production of IL-12 by APC and on the simultaneous up-regulation of IL-12R on Th cells rather than on an IL-2 autocrine mechanism.





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