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Mouse IL-17 Secretion Assay – Cell Enrichment and Detection Kit
Description
Interleukin 17 (IL-17) is a family of cytokines that play a central role in adaptive immunity as well as autoinflammatory disorders.1 Data from several mouse models suggest that IL-17 plays a key role in the host defense against certain extracellular bacterial infections.
Recently, a new mouse T helper cell subset has been identified, which is dinstinct from Th1 and Th2 cells: IL-17–producing CD4+ T helper (Th17) cells. Th17 cells preferentially produce IL-17A, IL-17F, IL-21, and IL-22. Receptors for IL-17 and IL-22 are expressed on various epithelial tissues, thus Th17 cells are crucial for the cross-talk between immune system and tissues.2 It is now established that Th17 cells are responsible for driving autoimmune inflammation.
After stimulation of mouse cells, IL-17 is not only secreted by CD4+ T cells, but also by CD8+ T cells, γδ T cells, NK cells, and granulocytes.
The Mouse IL-17 Secretion Assays allow the sensitive detection as well as enrichment of mouse IL-17A–secreting cells.
Applications
The Mouse IL-17 Secretion Assay – Cell Enrichment and Detection Kit can be used for the detection and enrichment of IL-17A–secreting mouse cells.
Columns
For positive selection using the Mouse IL-17 Secretion Assay – Cell Enrichment and Detection Kit: MS, LS, or autoMACS® Columns.
 
Figure 1
Figure 2
Mouse splenocytes were stimulated for 3 hours with ionomycin (1 μg/mL) and PMA (10 ng/mL) or left untreated. Cells were enriched by using the Mouse IL-17 Secretion Assay – Cell Enrichment and Detection Kit (PE). T helper cells were counterstained by using CD4-APC. B cells and dead cells were excluded from the analysis.
Stimulated sample
A: Before enrichment
B: After enrichment
Unstimulated control
A: Before enrichment
B: After enrichment
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Mouse IL-17 Secretion Assay – Cell Enrichment and Detection Kit (PE)
- for 50 tests with 107 total cells.
Download datasheet
130-094-213
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References
1. Weaver et al. (2007) Annu. Rev. Immunol. 25: 821–852.
2. Ouyang et al. (2008) Immunity 28: 454–467.
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