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 Blood, 7 May 2009, Vol. 113, No. 19, pp. 4534-4540.
Prepublished online as a Blood First Edition Paper on February 17, 2009; DOI 10.1182/blood-2008-12-192559.

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Submitted December 15, 2008
Accepted February 8, 2009

Interleukin 6 aborts lymphopoiesis and elevates production of myeloid cells in systemic lupus erythematosis-prone B6.Sle1.Yaa animals

Kenichiro Maeda, Alex Malykhin, Brittany N. Teague-Weber, Xiao-Hong Sun, A. Darise Farris, and K. Mark Coggeshall*

Program in Immunobiology & Cancer, Oklahoma Medical Research Foundation, Oklahoma City, OK, United States
Program in Arthritis & Immunology, Oklahoma Medical Research Foundation, Oklahoma City, OK, United States

* Corresponding author; email: mark-coggeshall{at}omrf.ouhsc.edu.

We previously reported the inhibitory action of IL-6 on B lymphopoiesis using SHIP-/- mice, and showed that IL-6 biases lineage commitment towards myeloid cell fates in vitro and in vivo. Since elevated IL-6 is a feature of chronic inflammatory diseases, we applied an animal model of systemic lupus erythematosus (SLE) to determine if IL-6 has similar effects on hematopoiesis. We found that IL-6 levels were elevated in the B6.Sle1.Yaa mice, and the increase was accompanied by losses of CD19+ B cells and more primitive B lymphoid progenitors in bone marrow. Both the CD19+ B cell population and their progenitors recovered in an IL-6-/- background. The uncommitted progenitors, containing precursors for both lymphoid and myeloid fates, expressed IL-6 receptor-{alpha} chain and responded to IL-6 by phosphorylation of STAT3. IL-6 stimulation caused uncommitted progenitors to express the Id1 transcription factor, which is known to inhibit lymphopoiesis and elevate myelopoiesis, and its expression was MAPK dependent. We conclude that chronic inflammatory conditions accompanied by increased IL-6 production bias uncommitted progenitors to a myeloid fate by inducing Id1 expression.


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