|| IL15; IL-15; MGC9721
| External IDs
|| OMIM: 600554 MGI: 103014 Homologene: 487
| Molecular Function:
|| • signal transducer activity|
• hematopoietin/interferon-class (D200-domain) cytokine receptor binding
• protein binding
| Cellular Component:
|| • extracellular region|
• extracellular space
• membrane fraction
• Golgi apparatus
• integral to plasma membrane
| Biological Process:
|| • NK T cell proliferation|
• immune response
• signal transduction
• cell-cell signaling
• positive regulation of cell proliferation
• positive regulation of T cell proliferation
• extrathymic T cell selection
• regulation of T cell differentiation
• lymph node development
• regulation of antiviral response by host
• positive regulation of immune response
| RNA expression pattern
Additional recommended knowledge
More reference expression data
|| NM_000585 (mRNA)|
|| Chr 4: 142.78 - 142.87 Mb
|| Chr 8: 85.23 - 85.24 Mb
| Pubmed search
Interleukin 15 (IL-15) is a cytokine with structural similarity to IL-2 that is secreted by mononuclear phagocytes (and some other cells) following infection by virus(es). This cytokine induces cell proliferation of natural killer cells; cells of the innate immune system whose principal role is to kill virally infected cells.
The protein encoded by this gene is a cytokine that regulates T and natural killer cell activation and proliferation. This cytokine and interleukine 2 share many biological activities. They are found to bind common hematopoietin receptor subunits, and may compete for the same receptor, and thus negatively regulate each other's activity. The number of CD8+ memory cells is shown to be controlled by a balance between this cytokine and IL2. This cytokine induces the activation of JAK kinases, as well as the phosphorylation and activation of transcription activators STAT3, STAT5, and STAT6. Studies of the mouse counterpart suggested that this cytokine may increase the expression of apoptosis inhibitor BCL2L1/BCL-x(L), possibly through the transcription activation activity of STAT6, and thus prevent apoptosis. Two alternatively spliced transcript variants of this gene encoding the same protein have been reported.
Maintenance of memory cells does not appear to require persistence of the original antigen; instead, survival signals for memory lymphocytes are provided by cytokines such as IL-15.
In transgenic mice that have the IL-15 receptor alpha (IL-15Ralpha) gene knocked out, natural killer cells cells do not develop.
In people with history of acute infectious mononucleosis (the syndrome associated with primary Epstein-Barr virus infection), IL-15R expressing lymphocytes are not detected--even 14 years after infection.
- ^ Entrez Gene: IL15 interleukin 15.
- Maślińska D (2001). "The cytokine network and interleukin-15 (IL-15) in brain development.". Folia neuropathologica / Association of Polish Neuropathologists and Medical Research Centre, Polish Academy of Sciences 39 (2): 43-7. PMID 11680634.
- Liew FY, McInnes IB (2002). "Role of interleukin 15 and interleukin 18 in inflammatory response.". Ann. Rheum. Dis. 61 Suppl 2: ii100-2. PMID 12379638.
- Lodolce JP, Burkett PR, Koka RM, et al. (2003). "Regulation of lymphoid homeostasis by interleukin-15.". Cytokine Growth Factor Rev. 13 (6): 429-39. PMID 12401478.