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Activation of JAK/STAT signaling results from association of cytokines to membrane-bound receptors, the engagement of which leads to the recruitment of JAKs to the intracellular face of the receptor. The integrity of this intramolecular interaction is central to preventing constitutive signaling by the JAK/STAT pathway. Figure7 binding of IL-6 leads to recruitment of JAK to the receptor which results in activation of STAT3. JAKs are preassembled into an inactive conformation which prevents association with cytokine or receptor. Phosphatases maintain this status. Figure8 association of IL-6 results in specific binding to the IL-6-specific receptor subunit gp130. Figure9 Association of IL-6 causes recruitment of JAKs to gp130. Figure10 gp130-specific antibody triggers dephosphorylation of STAT3.](pone.0030820.g007){#pone-0030820-g007}
Stat3 signals transcription by interacting with specific response elements. Repression of certain Stat3 target genes is due to repression of transcriptional factors that cooperate with Stat3 to induce transcription. For example, as noted in the previous review by Peehl and colleagues [36], the transcription factor c-myc can cooperate with Stat3 to drive oncogenic transcription in CML. Interestingly, c-myc is also a target of Stat3, leading to either repression or activation of target genes that are dependent upon Stat3-induced expression of c-myc. Loss of c-myc during B cell development is important for generation of B cells that are competent to enter germinal centers to undergo affinity maturation and class switching. However, deletion of c-myc leads to apoptosis in many B cell precursors, and loss of B cells due to this effect leads to reduced generation of Ab specific for antigen leading to defective germinal center responses. These results suggest that c-myc may cooperate with Stat3 to drive oncogenic transcription in B cells. Further investigation of c-myc and its downstream targets in CML and MDS/MPN may provide useful insights into how cytokine-induced Stat3 activation leads to deregulation of hematopoiesis and may provide novel therapeutic targets to treat MDS/MPN.
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