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KMID : 0391319980080010011
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Korean Journal of Biological Response Modifiers
1998 Volume.8 No. 1 p.11 ~ p.16
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IL-7, a key Cytokine in Lymphopoiesis
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김경재/Kyungjae Kim
이종길/Chong Kil Lee
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Abstract
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Numerous studies have shown that many cytokines provide proliferation and/or
differentiation signals for T or B cell precursors in vitro and in vivo. Thus, many
cytokines were once believed to participate in lymphopoiesis. Recent studies employing
targeted gene knock out mice, however, have shown that normal lymphopoiesis could
occur in mice lacking the respective cytokine or its receptor. The list of those cytokines
includes IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8, IL-12, IFNs, TNF-α, LT, TGFβ,
CSFs, erythropoietin, or thrombopoietin. This may reflect redundancy of cytokine
activity, one being dispensed by others. Meanwhile, targeted gene knock out studies
have clearly established that mutation of IL-7 or IL-7Rα results in severe defects in
both T and B-lymphopoiesis in mice.
IL-7 signals through a heterodimeric receptor complex composed of IL-7Rα and the
common γ chain(γc) of IL-2, IL-4, IL-7, IL-9, and IL-l5. The best characterized
downstream signaling element of the γc is Jak3 tyrosine kinase. Recently, mutant mice
lacking γc or Jak3 have also been generated, and have shown that they are severely
defective in both T and B-lymphopoiesis. Surprisingly, B cells, but not T cells, develop
almost normally in γc-deficient (XSCID) patients and humans with mutations in Jak.
This suggests that IL-7 is not required in human B cell development.
In this review, we will highlight the phenotype of IL-7 or IL-7R-deficient mice. Then,
the phenotype of IL-7Rα-deficient mice will be compared with that of γc or
Jak3-deficient mice to identify the IL-7 signaling pathway that is crucial in
lymphopoiesis. Finally, we will point out evidences that B cell development in human is
independent of IL-7 signaling.
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KEYWORD
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