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Abstract Number: 642

Treatment with a Glycolipid Ameliorates Lupus Dermatitis and Expands Skin ãä T Cells That Promote the Migration of Langerhans Dendritic Cells

Ram Raj Singh1,2,3, Anna Eriksson1, Darshan Randhawa1 and Miguel-Angel Gutierrez1, 1Autoimmunity and Tolerance Laboratory, Department of Medicine/Rheumatology, UCLA, Los Angeles, CA, 2Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA, 3Interdepartmental Program in Molecular Toxicology, UCLA, Los Angeles, CA

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: Dendritic cells, Lupus, lupus dermatitis and skin, T cells

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Session Information

Session Title: Systemic Lupus Erythematosus - Animal Models

Session Type: Abstract Submissions (ACR)

Background/Purpose: Self antigens are taken from tissues to local lymphoid organs to acquire ability to avoid self-reactivity.  This important immune function is accomplished by dendritic cell (DC) populations that primarily reside in tissues. We posit that a defect in the migration of tissue-resident DCs may predispose to autoimmunity in a tissue-specific manner; and an improved migration of tissue-specific DC may ameliorate disease in the respective organ. We have previously reported that lupus dermatitis-prone MRL mice exhibit a profound defect in the migration of skin-resident DC. Here, we investigated the effect of improved skin-DC migration on lupus dermatitis and determined mechanisms that regulate the migration of tissue-resident DC from tissues to lymph nodes

Methods: Skin and cutaneous lymph nodes from MRL-lpr mice and MHC-matched control mice and γδ T cell-deficient mice were analyzed for Langerhans DC and skin-resident invariant γδ T cells before and after treatment with a glycolipid αGalCer that was previously shown to ameliorate lupus dermatitis, without affecting disease in other organs.

Results: MRL mice that exhibit reduced skin-DC migration had reduced skin-resident γδ T cells, whereas treatment with αGalCer reduced the severity of lupus dermatitis and restored skin-γδ T cells and skin-DC migration. This effect of αGalCer was independent of its effect on invariant natural killer T cells, but required the presence of lipid antigen presenting molecule CD1d. We further show that gd T cell-deficient mice had reduced skin-DC migration in vivo, and skin-gd T cells directly promoted the migration of skin-DC in vitro via CD40L–CD40 interaction.

Conclusion: Our data elucidate a new mechanism of regulation of skin-DC homeostasis whereby skin-gd T cells normally facilitate skin-DC migration from skin to cutaneous lymph node. Such ‘local’ control of migratory behavior of tissue-DC can regulate immune response in a tissue-specific manner. This mechanism of skin-DC homeostasis is disrupted in lupus dermatitis, but can be repaired by treatment with a glycolipid.


Disclosure:

R. R. Singh,
None;

A. Eriksson,
None;

D. Randhawa,
None;

M. A. Gutierrez,
None.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/treatment-with-a-glycolipid-ameliorates-lupus-dermatitis-and-expands-skin-aa-t-cells-that-promote-the-migration-of-langerhans-dendritic-cells/

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