HIGHLIGHTS
SUMMARY
The mechanisms contributing to the low expression Th2 model in asthmatic patients are less clear: dysregulated neutrophil-mediated immune_responses due to respiratory infections or defects in resolution of inflammation, and the activation of the IL-17-dependent pathway have been proposed as possible mechanisms involved. During asthma exacerbations the cytokines IL-8 and IL-17A prolong the life span of the neutrophil and modulates Th2 and innate immune_responses. Because of their longer lifespan, neutrophils can move from tissues to the bloodstream or lymph nodes to influence adaptive immune_responses. A lack of allergy history, negative . . .
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