Capsiate Inhibits DNFB-Induced Atopic Dermatitis in NC/Nga Mice through Mast Cell and CD4+ T-Cell Inactivation

AbstractTfh initiates four eradicable immunities. Tfh includes FDC, LTi, IL21 CD4 T cell, and IgG/M B cell. Treg initiates four tolerable immunities. Treg includes DCreg, ILCreg, TGFβ CD4 T cell, and IgA B cell. TH1/TH1-like is immunity for intracellular bacteria/protozoa and type 4 delayed type hypersensitivity. TH1 includes M1 macrophage, mDC2, Tc1 CD8 T cell, IFNg CD4 T cell, ILC1, iNKT1, and IgG3 B cell. TH1-like includes M2 macrophage, ILC1, suppressive CD8 T cell, IFNg/TGFβ CD4 T cell, regulatory iNKT cells, and IgA1 B cell. TH2/TH9 is immunity for helminths and type1 IgE mediated hypersensitivity. TH2 includes iEOS eosinophil, Langerhans cell, basophil/MCt mast cell, IL-4 CD4 T cell, ILC2, iNKT2, and IgE/IgG4 B cell. TH9 includes rEOS eosinophil, basophils/mast cell MCct, IL-9 CD4 T cell, ILC2, regulatory iNKT cells, and IgA2 B cell. TH22/TH17 is immunity for extracellular bacteria/fungi and type 3 immune complex hypersensitivity. TH22 includes N1 neutrophils, mDC1, IL-22 CD4 T cell, ILC3(NCR+), iNKT17, and IgG2 B cell. TH17 includes N2 neutrophils, IL-17 CD4 T cell, regulatory iNKT cells, ILC3(NCR−), and IgA2 B cell. THαβ/TH3 is immunity for viruses and type 2 antibody dependent cytotoxic hypersensitivity. THαβ includes NK1 natural killer cell, pDC, Tc2 CD8 T cell, IL10 CD4 T cell, ILC10, iNKT10, and IgG1 B cell. TH3 includes NK2 natural killer cell, suppressive CD8 T cell, ILC10, IL-10/TGFβ CD4 T cell, regulatory iNKT cells, and IgA1 B cell.Summary sentenceThe summarized framework of host immunities to explain their relations to specific pathogens and hypersensitivities

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CX3CL1 (fractalkine) and its receptor CX3CR1 regulate atopic dermatitis by controlling effector T cell retention in inflamed skin

Journal of Experimental Medicine ◽

10.1084/jem.20121350 ◽

2014 ◽

Vol 211 (6) ◽

pp. 1185-1196 ◽

Cited By ~ 23

Author(s):

Delphine Staumont-Sallé ◽

Sébastien Fleury ◽

Anne Lazzari ◽

Olivier Molendi-Coste ◽

Nicolas Hornez ◽

...

Keyword(s):

Atopic Dermatitis ◽

T Cell ◽

Chemokine Receptors ◽

Allergic Diseases ◽

Experimental Models ◽

Cd4 T Cell ◽

Cell Retention ◽

T Cell Survival ◽

Receptor Cx3cr1

Atopic dermatitis (AD) is a chronic allergic dermatosis characterized by epidermal thickening and dermal inflammatory infiltrates with a dominant Th2 profile during the acute phase, whereas a Th1 profile is characteristic of the chronic stage. Among chemokines and chemokine receptors associated with inflammation, increased levels of CX3CL1 (fractalkine) and its unique receptor, CX3CR1, have been observed in human AD. We have thus investigated their role and mechanism of action in experimental models of AD and psoriasis. AD pathology and immune responses, but not psoriasis, were profoundly decreased in CX3CR1-deficient mice and upon blocking CX3CL1–CX3CR1 interactions in wild-type mice. CX3CR1 deficiency affected neither antigen presentation nor T cell proliferation in vivo upon skin sensitization, but CX3CR1 expression by both Th2 and Th1 cells was required to induce AD. Surprisingly, unlike in allergic asthma, where CX3CL1 and CX3CR1 regulate the pathology by controlling effector CD4+ T cell survival within inflamed tissues, adoptive transfer experiments established CX3CR1 as a key regulator of CD4+ T cell retention in inflamed skin, indicating a new function for this chemokine receptor. Therefore, although CX3CR1 and CX3CL1 act through distinct mechanisms in different pathologies, our results further indicate their interest as promising therapeutic targets in allergic diseases.

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