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Effects of interleukin-11 on the proliferation and cell cycle status of myeloid leukemic cells
| Content Provider | Scilit |
|---|---|
| Author | Hu, Jp Cesano, A. Santoli, D. Clark, Sc Hoang, T. |
| Copyright Year | 1993 |
| Description | Interleukin-11 (IL-11) is a pleiotropic cytokine with effects on many different targets. Within the hematopoietic system, the effects of IL- 11 are largely manifest only through combination with other cytokines, including IL-3 and Steel factor (SF). In the present study, we addressed the question of IL-11 responsiveness within the different types of human leukemic cells, as well as the mechanism of action of IL- 11 at the cellular level. Analysis of a panel of samples from different patients with acute myeloblastic leukemia (AML) and myeloid leukemic cell lines indicated that IL-11 alone was ineffective in supporting myeloid leukemic cell growth but frequently enhanced growth supported by IL-3, granulocyte-macrophage colony-stimulating factor (GM-CSF), or SF. In contrast, three acute pre-B lymphocytic leukemia (pre-B-ALL) and two acute T lymphocytic leukemia (T-ALL) lines failed to respond to IL- 11 alone or when combined with other cytokines. The growth enhancement of IL-11 among the AML patient samples was dose dependent and remarkably constant with half-efficient concentrations in the range of 0.3 to 0.4 ng/mL. The thymidine suicide studies with the patient samples revealed that 40% to 50% of the blast cells were in S-phase when exposed for 16 hours to IL-3 and this level was increased to 70% to 90% in response to either IL-11 or IL-6. Our data suggest that the latter two interleukins act synergistically with the direct mitogenic factor, IL-3, in triggering AML blast-cell proliferation. Detailed analysis with several patient samples further revealed that SF and IL- 11 both enhance IL-3-supported clonogenic growth of AML blasts and the combination of all three growth factors yields optimal growth. In contrast, IL-6 does not further enhance the effect of IL-11. These results indicate that SF and IL-11 enhance IL-3-dependent clonogenic growth through two distinct pathways, whereas IL-6 and IL-11 may trigger the same pathway. |
| Related Links | https://ashpublications.org/blood/article-pdf/81/6/1586/610105/1586.pdf |
| Ending Page | 1592 |
| Page Count | 7 |
| Starting Page | 1586 |
| DOI | 10.1182/blood.v81.6.1586.1586 |
| Journal | Blood |
| Issue Number | 6 |
| Volume Number | 81 |
| Language | English |
| Publisher | American Society of Hematology |
| Publisher Date | 1993-03-15 |
| Access Restriction | Open |
| Subject Keyword | Biochemistry and Molecular Biology Hematology Cell Proliferation Hematopoietic Aml Leukemia Optimal Blast Myeloid Leukemic Journal: Blood (Vol- 89, Issue- 6) |
| Content Type | Text |
| Resource Type | Article |
