Interleukin‐13 is produced by activated human CD45RA+ and CD45R0+ T cells: modulation by interleukin‐4 and interleukin‐12

T Jung, J Wijdenes, C Neumann… - European journal of …, 1996 - Wiley Online Library
T Jung, J Wijdenes, C Neumann, JE de Vries, H Yssel
European journal of immunology, 1996Wiley Online Library
Abstract Interleukin (IL)‐13 is a cytokine originally identified as a product of activated T cells.
Little is known, however, about IL‐13 production by human T cells and its modulation by
other cytokines. Here, we show that IL‐13 is produced by activated human CD4+ and CD8+
CD45R0+ memory T cells and CD4+ and CD8+ CD45RA+ naive T cells. In contrast, IL‐4,
which shares many biological activities with IL‐13, is only produced by CD45R0+ T cells
following activation. Analysis of intracellular cytokine production by single CD45RA+ and …
Abstract
Interleukin (IL)‐13 is a cytokine originally identified as a product of activated T cells. Little is known, however, about IL‐13 production by human T cells and its modulation by other cytokines. Here, we show that IL‐13 is produced by activated human CD4+ and CD8+ CD45R0+ memory T cells and CD4+ and CD8+ CD45RA+ naive T cells. In contrast, IL‐4, which shares many biological activities with IL‐13, is only produced by CD45R0+ T cells following activation. Analysis of intracellular cytokine production by single CD45RA+ and CD45R0+ T cells indicated that IL‐13 continued to be produced for more than 24 h after stimulation, whereas IL‐4 could not be detected after 24 h. These data were confirmed by measurement of specific mRNA and suggest that IL‐13, unlike IL‐4, but like interferon‐γ (IFN‐γ), is a cytokine with long‐lasting kinetics. The majority of human CD45R0+ T cells produced IL‐4 and IL‐13 simultaneously. In contrast, IFN‐γ protein was generally not co‐expressed with IL‐4 or IL‐13. IL‐4 added to primary cultures of highly purified peripheral blood T cells activated by the combination of anti‐CD3+anti‐CD28 mAb enhanced IL‐13 production by CD45RA+ and to a lesser extent by CD45R0+ T cells. Under these conditions, however, IL‐12 inhibited IL‐13 production by CD45RA+ T cells and to a lesser extent by CD45R0+ T cells in a dose‐dependent fashion. These inhibiting effects were not related to enhanced IFN‐γ production induced by IL‐12, since IFN‐γ by itself did not affect IL‐13 production. Collectively, our data indicate that IL‐13 is produced by peripheral blood T cells which also produce IL‐4, but not IFN‐γ, and by naive CD45RA+ T cells which, in contrast, fail to produce IL‐4. These observations, together with the long‐lasting production of IL‐13, suggest that IL‐13 may have IL‐4‐like functions in situations where T cell‐derived IL‐4 is still absent or where its production has already been down‐regulated.
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