Therefore, this study examined the regulatory roles of CTH and MPST in experimental colitis induced by different model haptens, trinitrobenzene sulfonic acid (TNBS) and oxazolone, as mucosal immunity models [13], and experimental contact dermatitis induced by trinitrochlorobenzene (TNCB) and oxazolone, as systemic immunity models, using the previously established CTH-deficient (Cth–/–) and MPST-deficient (Mpst–/–) mice [14,15]. The gene discussed is MPST; the disease is contact dermatitis.