Table 4.
The inflammasome in vitiligo and AD.
| Activator | Implicated genetic component | Cell type | Effector signal | Mouse model | Main findings | References |
|---|---|---|---|---|---|---|
| The NLRP3 inflammasome in vitiligo | ||||||
| Monobenzone | Asc | Natural killer cells, Macrophages, Dendritic cells | na | Rag2−/−, P2rx7−/−, Nlrp3−/−, Asc−/−, IL18−/− | Monobenzone-induced memory natural killer cell formation is dependent on the NLRP3 inflammasome of macrophages. | (108) |
| H2O2 | Trpm2, ROS, NF-κB, Cxcl10, Cxcl16, Trpm2, Irf1, Asc, Casp1 | T cells, NHEK | na | na | Oxidative stress–induced NLRP3 inflammasome activation in keratinocytes promotes cutaneous T-cell responses in vitiligo. | (109) |
| The NLRP3 inflammasome in AD | ||||||
| Staphylococcal alpha-toxin | Il4, Il5, Il13, Il17, Il22, Ifng, Casp1, Asc | Monocytes, Keratinocytes | IL-1β | Na | Impaired NLRP3 expression and function may be important for Staphylococcus aureus-induced chronic skin inflammation in AD. | (110) |
| Dermatophagoides pteronyssinus | Asc, Casp1, NF-κB, Il8 | Keratinocytes | IL-1β, IL-18 | Na | House dust mite allergens activate the NLRP3 inflammasome in the development of atopic dermatitis. | (111) |
| Ultraviolet B irradiation | Il18bp, Tslp | na | IL-18 | NC/Nga | The NLRP3 inflammasome is implicated in the effects of UVB irradiation. | (112) |
| Hemolysins, Lipoproteins | Nlrc4, P2rx7r, Asc, Lta, Casp1 | Macrophages | IL-1β | Nlrp3−/−, Asc−/−, Casp1−/−, P2rx7r−/−, Trif−/− | S. aureus hemolysins circumvent the requirement for ATP and the P2rx7 receptor to induce caspase-1 activation via the NLRP3 inflammasome. | (113) |
AD, atopic dermatitis.