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  • Correspondence
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TSLP-mediated fetal B lymphopoiesis?

Nature Immunology volume 8, page 897 (2007)Cite this article

A Correspondence to this article was published on 01 September 2007

To the editor:

In the August 2003 issue of Nature Immunology1, as well as in later studies2, Voβhenrich et al. presented experimental data on the cytokine requirements of developing B cells, which led them to conclude that “TSLP [thymic stromal lymphopoietin] is the factor responsible for most of the fetal and perinatal B cell production that takes place when the IL-7–γc [interleukin 7–common γ-chain] signaling pathway is disrupted.”1 Although the data reported were technically sound and compatible with such a conclusion, the authors did not provide direct evidence to support (or exclude) the idea of a critical function for TSLP in IL-7-independent fetal B lymphopoiesis. The conclusions of Voβhenrich et al. were based on the demonstration that B lymphopoiesis was much more affected (tenfold more) in mice deficient in IL-7 receptor α-chain, essential for IL-7 as well as TSLP signaling, than in mice deficient in the common γ-chain (γc), required for IL-7 but not TSLP-mediated signaling3,4. However, these data could at best be considered strong indirect support for the idea of TSLP as the main cytokine driving IL-7-independent fetal B lymphopoiesis, as there could be other reasons for a difference in the phenotypes of γc-deficient mice and those deficient in the IL-7 receptor α-chain. Furthermore, Voβhenrich et al. used bone marrow of mice 4–12 weeks of age, not fetal liver, for their comparative in vivo analysis of B lymphopoiesis in these mice1,2. Instead, the extrapolation to the idea that TSLP is key to the fetal stages of B lymphopoiesis was based on the finding that fetal but not adult pro–B cells were responsive to TSLP in vitro1,2. In contrast, a lack of an important function for TSLP in adult B lymphopoiesis has been indicated by studies of TSLP receptor–deficient (Tpte2−/−) mice5,6.

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Figure 1: Critical function for IL-7 but not TSLP in the regulation of fetal B cell progenitors.

References

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Authors and Affiliations

  1. Hematopoietic Stem Cell Laboratory, Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Lund University, Lund, 221 84, Sweden

    Christina T Jensen, Shabnam Kharazi, Charlotta Böiers, Karina Liuba & Sten Eirik W Jacobsen

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  1. Christina T Jensen
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  2. Shabnam Kharazi
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  3. Charlotta Böiers
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  4. Karina Liuba
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  5. Sten Eirik W Jacobsen
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Jensen, C., Kharazi, S., Böiers, C. et al. TSLP-mediated fetal B lymphopoiesis?. Nat Immunol 8, 897 (2007). https://doi.org/10.1038/ni0907-897

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