Abstract
CX3CL1 can function as both an adhesion molecule and a chemokine for CX3CR1+ cells, such as T cells, monocytes, and NK cells. Recent studies have demonstrated that CX3CL1–CX3CR1 interaction is associated with the development of various inflammatory skin diseases. In this study, we examined CX3CR1 involvement in 2,4-dinitrofluorobenzene (DNFB)-induced contact hypersensitivity using CX3CR1−/− mice. Ear swelling and dermal edema were attenuated after DNFB challenge in CX3CR1−/− mice. Expression of TNF-α, IL-6, and M1 macrophage markers was decreased in the ears of CX3CR1−/− mice, whereas expression of M2 macrophage markers including arginase-1 was increased. Decreased TNF-α and IL-6 expression and increased arginase-1 expression were found in peritoneal macrophages from CX3CR1−/− mice. Furthermore, ear swelling was attenuated by depleting dermal macrophages in wild-type mice to a similar level to CX3CR1−/− mice. These results suggest that CX3CR1 deficiency could induce skewed polarization towards M2 phenotype in macrophages, resulting in attenuation of contact hypersensitivity response.
Highlights
Contact hypersensitivity (CHS) is a cutaneous immunological response against a small chemical hapten including 2,4-dinitrofluorobenzene (DNFB), fluorescein isothiocyanate, and oxazolone
Depletion of dermal macrophages did not affect the ear swelling of CX3CR1−/− mice after DNFB challenge (Figure 5). These results suggest that macrophages play an important role in DNFB-induced CHS response and that macrophages with downregulated inflammatory cytokines and upregulated arginase-1 in CX3CR1−/− mice are involved in attenuation of DNFB-induced CHS response
We first showed that CHS response by DNFB was attenuated in CX3CR1−/− mice compared with wild-type mice
Summary
Contact hypersensitivity (CHS) is a cutaneous immunological response against a small chemical hapten including 2,4-dinitrofluorobenzene (DNFB), fluorescein isothiocyanate, and oxazolone. Various allergens such as metals, plants, and drugs can cause allergic contact dermatitis [1,2]. T cells cause injury to the skin via production of inflammatory cytokines and activation of other immune cell populations, such as NK cells and macrophages In this context, chemokines and chemokine receptors are deeply involved in the process of CHS via trafficking of antigen-presenting cells to the lymph node and recruiting of inflammatory cells to the hapten-applied site [5]. CXCR3-deficient regulatory T cells have less capacity to produce suppressive cytokines, such as interleukin (IL)-10 and transforming growth factor-β; DNFB-induced CHS was prolonged in CXCR3−/− mice [6]
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