2016
DOI: 10.21037/atm.2016.11.79
|View full text |Cite
|
Sign up to set email alerts
|

Do insights from mice imply that combined Th2 and Th17 therapies would benefit select severe asthma patients?

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1

Citation Types

0
4
0

Year Published

2017
2017
2020
2020

Publication Types

Select...
4

Relationship

0
4

Authors

Journals

citations
Cited by 4 publications
(4 citation statements)
references
References 19 publications
(14 reference statements)
0
4
0
Order By: Relevance
“…Although IL-17 is most richly expressed by 17 cells, it can also be produced by other immune cells, including macrophages, B cells, natural killer T cells, innate lymphocytes, and CD8+T cells [54]. Indeed, IL-17 and 17 cells have been shown to be associated with human autoimmune diseases in many tissue regions, including psoriasis, rheumatoid arthritis, inflammatory bowel disease, systemic lupus erythematosus, and asthma [55][56][57][58][59][60][61]. Recent evidence suggests that 17 cells are also associated with 2 hypersensitivity [62,63].…”
Section: And Il-7 May Promote Acmentioning
confidence: 99%
“…Although IL-17 is most richly expressed by 17 cells, it can also be produced by other immune cells, including macrophages, B cells, natural killer T cells, innate lymphocytes, and CD8+T cells [54]. Indeed, IL-17 and 17 cells have been shown to be associated with human autoimmune diseases in many tissue regions, including psoriasis, rheumatoid arthritis, inflammatory bowel disease, systemic lupus erythematosus, and asthma [55][56][57][58][59][60][61]. Recent evidence suggests that 17 cells are also associated with 2 hypersensitivity [62,63].…”
Section: And Il-7 May Promote Acmentioning
confidence: 99%
“…The authors propose that in asthma, a predisposition to T2 inflammation is driven towards T17-mediated inflammation by corticosteroid therapy [128]. This hypothesis would have important implications for patients receiving type 2-targeting biologics, although the study has provoked some controversy [129,130].…”
Section: Is There a Reciprocal Relationship Between T2 And T17 Inflammation?mentioning
confidence: 99%
“…There are as yet no prospective clinical data showing development of T17 inflammation in people receiving blockade of T2 pathways. Whether such an increase T17 inflammation would be harmful is also unknown [130], and will be important to investigate.…”
Section: Is There a Reciprocal Relationship Between T2 And T17 Inflammation?mentioning
confidence: 99%
“…In addition, granulocyte colony-stimulating factor and GM-CS, but not IL-17A, levels were increased in patients with T H 2/T H 17-low asthma, raising the possibility that these cytokines might also be inhibited by IL-4 or some other factor produced by T H 2 cells. Early clinical studies blocking IL-4 and/or IL-13 signaling have not yet been noted to result in a neutrophilic airway phenotype 10 ; however, the possibility that T H 2 cytokines might inhibit neutrophil recruitment is plausible based on the studies described above, and there needs to be vigilance that such phenotypes do not develop with the use of pharmacologic agents that antagonize the IL-4/IL-13 production or signaling axis. Although there is associative evidence that IL-17 might be involved in asthma pathogenesis, inhibition of IL-17 signaling with an IL-17 receptor antagonist did not improve asthma outcomes, 11 therefore pinpointing a biomarker that identifies who might have T H 17driven asthma pathogenesis is critical to determine the patient population those would benefit from either a more potent IL-17 antagonist or dual T H 2/T H 17 antagonism.…”
mentioning
confidence: 99%