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Th17 profile in COPD exacerbations

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Figure 1 When airway epithelium is exposed to harmful substances, such as those contained in cigarette smoke, it changes its structure.Note: These changes include the loss of close junctions between ciliated epithelial cells, shortening of cilia, hyperplasia of goblet-producing goblet cells and basal cells, in addition to squamous epithelial cell metaplasia.Abbreviation: DAMPs, damage-associated molecular patterns.
Figure 2 With exposure to harmful agents, epithelial cells present in the airways release DAMPs, such as HSPs that are recognized by membrane receptors (TLRs, for example) present in leukocytes, such as DCs.Note: This leads to an intracellular signaling cascade commanded by MyD88 and the transcription factor NF-κB, culminating in the release of proinflammatory cytokines such as IL-1β and IL-18, important mediators in the pathophysiology of COPD.Abbreviations: DAMPs, damage-associated molecular patterns; HSP, heat shock protein; TLR, Toll-like receptor; DC, dendritic cell; HMGB1, high mobility group box 1; IL, interleukin.
Figure 3 When dendritic cells pick up DAMPs, they travel to the lymph nodes where they are presented to the virgin T lymphocytes through the class II MHC-11, which binds to the TCR present on the cell membrane.Notes: Along with the existing cytokine microe
Table 1 Principal characteristics of cytokines related with Th17 lymphocytes
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