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Adhesion molecules are critical for leukocytes migration to the skin. Leukocytes must first be captured or tethered from the flowing blood allowing them to roll along the skin vessels. Leukocytes are activated by chemoattractants, which results in firm adhesion and arrest and ultimately transendothelial migration into the tissue. Selectin family which consists of L-selectin, P-selectin, E-selectin is critical for capture and rolling. Deficiency of these molecules leads to the diminution of cutaneous inflammation. Firm adhesion is governed by β2 integrin and α4 integrin. Inhibition of β2 integrin and its ligand ICAM-1 also reduce cutaneous inflammation. Similarly, blocking of α4 integrin and its ligand VCAM-1 alleviate inflammation of the skin. Transmigration and diapedesis are mediated by various molecules such as PECAM-1, CD99, and JAM, whose inhibition also leads to amelioration of skin inflammation. Manipulating adhesion molecules might lead to novel therapy to treat dermatitis by controlling leukocytes migration into cutaneous sites of inflammation.

The role of adhesion molecules in cutaneous inflammation