Pierce, A and Whetton, A D and Owen-Lynch, P J and Tavernier, J and Spooncer, E and Dexter, T M and Heyworth, C M (1998) Ectopic interleukin-5 receptor expression promotes proliferation without development in a multipotent hematopoietic cell line. Journal of Cell Science, 111 (6). pp. 815-823. ISSN 0021-9533Full text not available from this repository.
The interleukin-5 (IL-5) receptor is a heterodimer that consists of an IL-5 specific alpha subunit and a common ssc chain that is shared with the receptors for granulocyte macrophage colony stimulating factor (GM-CSF) and interleukin-3 (IL-3). In contrast to IL-5, which acts mainly as an eosinophil lineage specific factor in vivo, IL-3 and GM-CSF stimulate the survival, proliferation and development of various hematopoietic cell lineages and also multipotent progenitor cells. IL-5 has little effect on the survival or proliferation of the multipotent stem cell line FDCP-Mix A4 but does promote some eosinophil development. To investigate whether the lineage specificity of IL-5 is due to the restricted expression of the IL-5 receptor alpha subunit we transfected the FDCP-Mix A4 cells with a retroviral vector containing this alpha subunit. The ectopic expression of the IL-5 receptor alpha subunit in the FDCP-Mix cells did not increase the observed eosinophilic development but did stimulate survival and proliferation of the transfected cells when IL-5 was added. IL-5 thus acts like IL-3 in these cells, promoting proliferation and survival. The results suggest that IL-5, whilst having a capacity to promote proliferation, does not influence eosinophilic lineage commitment in these multipotent cells. The results further argue that the observed lineage specificity of IL-5 is probably due to factors in addition to the restricted expression of the IL-5 receptor alpha subunit.
|Journal or Publication Title:||Journal of Cell Science|
|Subjects:||Q Science > QR Microbiology|
|Departments:||Faculty of Health and Medicine > Biomedical & Life Sciences|
|Deposited On:||24 Jul 2012 11:18|
|Last Modified:||20 Feb 2017 03:18|
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