Hapten-Induced Contact Hypersensitivity, Autoimmune Reactions, and Tumor Regression: Plausibility of Mediating Antitumor Immunity

Figure 2

The likely pathway of the “early elicitation” phase of contact hypersensitivity. The red arrows and type indicate the early elicitation phase. Hapten challenge will restimulate iNKT cells to release IL-4, which along with hapten-antigen will stimulate CS-initiating B-1 cells as seen in Figure 1. These cells will release IgM, which will bind to hapten-antigen. This will cause formation of C5a, triggering activation of mast cells to produce TNFα and serotonin, increasing immune cell trafficking into the area and TNFα and CXCL2 to stimulate neutrophils in the dermis. Neutrophils will also be activated by CXCL1 and CXCL2 released from haptenation of the keratinocytes. Their activation will cause damage at the challenge site as well as more CXCL1 and CXCL2 release, inducing immune cell trafficking to the area as illustrated in Figure 3. Lastly, haptenated keratinocytes will release cytokines to induce immune cell trafficking to the area as depicted in Figure 3.