FIGURE 1 | Innate recognition of haptens.

From the following article:

Early immune events in the induction of allergic contact dermatitis

Daniel H. Kaplan, Botond Z. Igyártó & Anthony A. Gaspari

Nature Reviews Immunology 12, 114-124 (February 2012)

doi:10.1038/nri3150

Early immune events in the induction of allergic contact dermatitis

The earliest event in allergic contact dermatitis is the formation of hapten–self complexes. Complete haptens, such as dinitrofluorobenzene (DNFB), are directly reactive with protein nucleophiles and can form a complex without prior modification. Pre-haptens, such as the fragrance limonene, are activated by oxidation before skin contact. Pro-haptens, such as urushiol (a molecule found in poison ivy), are activated enzymatically once on the skin. Through a poorly described process, haptens induce the production of reactive oxygen species (ROS), which lead to the release of ATP and possibly other damage-associated molecular patterns (DAMPs), as well as to the generation of low-molecular-weight hyaluronic acid. Low-molecular-weight hyaluronic acid is sensed by neighbouring cells via Toll-like receptor 2 (TLR2) and TLR4, resulting in increased expression of inactive pro-interleukin-1β (pro-IL-1β) and pro-IL-18. ATP is sensed through the purinergic receptor P2X7 and activates the inflammasome, resulting in caspase 1 activity and the generation of active IL-1β and IL-18. Nickel has a unique adjuvant property and can directly bind to histidine residues in the extracellular domain of TLR4, triggering the activation of this receptor. IRF3, IFN-regulatory factor 3; NF-κB, nuclear factor-κB; NLRP3, NOD-, LRR- and pyrin domain-containing 3; TRIF, TIR-domain-containing adaptor protein inducing IFNβ.

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