Kinetic profiles of sequential gene expressions for chemokines in mice with contact hypersensitivity

Effect of a topical steroid on gene expressions for chemokines in mice with contact hypersensitivity

“…All of the chemokine mRNA expressions examined were up-regulated from 3 to 6 h post-challenge, and although the ear swelling response attenuated with time at 48 and 72 h, some of the chemokine mRNAs were still clearly expressed. This suggests that a sequential and coordinated expression of chemokine genes is essential to maintain the CHS response [17,34]. As reported previously [35 -37], when the ointment of diflucortolone valerate, a synthetic corticosteroid, was topically applied in this model, ear swelling was completely suppressed with inhibited infiltration of inflammatory cells in the dermis.…”

Characterization of a murine keyhole limpet hemocyanin (KLH)-delayed-type hypersensitivity (DTH) model: Role for p38 kinase

“…A contributing factor to the differential infiltration of CD4+ and CD8+ T cell in these models may be reflected by the differences in mediator profiles. While mediators such as IL-1β, IL-10, TNFα, CCL2 and CXCL10 play a role in both models [5,[82][83][84], several molecules such as IFNγ, IL-3, IL-13, CXCL9, CXCL11, CCL1, CCL5, CCL7, CCL12, and GM-CSF are induced in the DNFB model [5,9,82,83] but are not markedly elevated in the ear parenchyma in our DTH model. The less expansive mediator composition and differing lymphocyte profiles in the KLH-DTH compared to the DNFB-CHS response may contribute to differential effects of immunomodulators in these two responses.…”

Macrophages and neutrophils are the targets for immune suppression by glucocorticoids in contact allergy

“…IP-10 is also known to be required for a complete induction of CHS because the IP-10-knockout mice show a reduced swelling response (13,47). IP-10 is induced during the challenge phase in keratinocytes and monocytic cells in the skin (48). Activated infiltrating T cells express CXCR3, the receptor for IP-10 (49), thus linking increased expression of IP-10 to the recruitment of sensitized T cells to the site of inflammation.…”