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About CCL22 / MDC:

CL22 (chemokine) is part of a group of heparin binding proteins that can induce migration and extravasation of chronically activated Th2 cells into the skin. They also create their own action via binding to G protein-coupled receptor CCR4, which then increases the intracellular Ca++ mobilization that can affect the cytoskeleton-induced movement, while boosting the affinity of specialist targeted cells to join to molecules.

Adhesion molecules, E-selectin and intercellular adhesion molecule 1 are upregulated when it comes to the dermal post capillar venules caused by cytokines released by antigen, a skin resident presenting cells such as Langerhans dendritic cells. These cells can also create activated T cell chemokines, including CCL22 on local endothelium which can result in the collection of cutaneous leukocyte antigen positive and chemokine receptor 4 positive.

Within the skin, T cells come across their cognate antigen specific Langerhans dendritic cells. Because of this, they are activated and begin to expand to suppress activation and proliferation of effector T cells. This group of suppressive T cells is not allowed in skin autoimmune diseases treated by Corticosteroids, Calcineurin inhibitors and Vitamin D3, this is due to the fact that they induce IL-10 expression which can inhibit CCL22 production by skin dendritic cells.

CCL22 was discovered in macrophages, however it is also a produced by activated B lymphocytes and dendritic cells. This cell is also present in mice. In humans, CCL22 is found as part of a mini cluster in chromosome 16q13, close to gene CCL17, with both Chemokines having homeostatic and anti inflammatory values. Both CCL22 and CCL17 bind the same receptor, CCR4, and can induce Ca++ mobilization and chemo-attracting action on Th2 lymphocytes. However, they also have a preferential effect on CD4+ regulatory T lymphocytes.

CCL2 is expressed in dendritic cells, B cells and also macrophages, whereas NK cells, monocytes and CD4 lymphocytes express CCL22 only after stimulation. Langerhans dendritic cells, which are known as skin-epidermis populated immature dendritic cells, are also able to express CCL22, but only once they have matured. However, in mice, this gene is expressed most abundantly.
When langerhans come across antigen in the epidermis, they begin to drain to the skin regional lymph node in response to coming across CCL21. In the lymph node, langerhans Dendritic cells offer antigen naive T cells to turn into effector memory T cells that express CLA and CCR4 (the CCL22 receptor) besides the central memory T cells which reside in skin lymphoid organ and express E-selectin and CCR7. However, there are other pathways for moving Langerhans dendritic cells. Once these cells come across their second antigen encounter, the effector memory T cells home to skin in antigen nonspecific manner from regional skin lymph node via chemokine mediated homing.
Immunogenic action of langerhans cells has been suggested, their tolerogenic work is still in an early stage. Ralph M Steinman shared the Nobel Prize in 2011 due to his work on dendritic cells and their role in health immunity. He found the role of dendritic cells in peripheral tolerance by adding antigen in absence of danger signal. This work gave the second wing for dendritic cells and open the door to better understand the role of homeostasis of the immune system.