Expression of CS‐1 fibronectin precedes monocyte chemoattractant protein‐1 production during elicitation of allergic contact dermatitis

Abstract

We showed evidence of the fact that CS-1 fibronectin expression precedes the production of MCP-1/CCL2 and TARC/CCL17 in the skin of patients with ACD, suggesting that these molecules participate in the early complex process of migrating mononuclear cells during elicitation of ACD.

Synergy‐inducing chemokines enhance CCR2 ligand activities on monocytes

“…Of note, this synergism occurs also in the opposite direction: CCL7 synergizes with CCL19 and CCL21 on CCR7-transfected cells as well as on mature dendritic cells, as we previously described [9]. A meeting place of both homeostatic and inflammatory chemokines is HEV where CCL19 and CCL21 are both expressed [26], and CCL2 and CCL7 [20,42] are transported from inflamed tissue to trigger arrest of rolling monocytes [32]. Therefore, the CCR7 and the CCR2 agonists meet the criteria to be at the same place and at the same time to enhance the migration of CCR2 1 cells in vivo.…”

“…Most leukocytes express more than one chemokine receptor and, hence, can respond to more than one chemokine. Additionally, a great variety of in situ experiments demonstrated the concomitant expression of chemokines at target sites of leukocyte trafficking and homing [16][17][18][19][20][21].…”

“…Most leukocytes express more than one chemokine receptor and, hence, can respond to more than one chemokine. Additionally, a great variety of in situ experiments demonstrated the concomitant expression of chemokines at target sites of leukocyte trafficking and homing [16][17][18][19][20][21].Many chemokines, apart from being agonistic for their receptors, were shown to act as natural antagonists on one or several receptors in vitro and in vivo [22]. Naturally occurring N-terminal truncations of chemokines have been identified in vivo [23] and numerous enzymes were shown to generate truncations of chemokines that render them less active or inactive [24,25].…”

“…In lymph nodes, HEV could be the meeting place of CCL19 or CCL21 and inflammatory chemokines such as CCL2 or CCL7. For example, CCL2 is produced upon allergen exposure in contact dermatitis [20] and is transported from inflamed tissue to the draining lymph node where it is exposed on the luminal surface of HEV to trigger arrest of rolling monocytes [32]. Therefore, these chemokines meet the criteria in vivo to be at the same place and at the same time to enhance the migration of CCR2 1 cells.…”

Comparative Study of Systemic Inflammatory Responses in Psoriasis Vulgaris and Mild to Moderate Allergic Contact Dermatitis

“…Contact allergens and irritants can directly induce the expression of both TNF-α and MCP-1 [23] that may explain increased serum levels of these cytokines in patients with ACD. For example, Martin et al [24] have demonstrated the expression of MCP-1 by basal keratinocytes and isolated dermal cells at 10 h after antigen challenge, paralleled by dermal accumulation of mononuclear cells. TNF-α may contribute to the rise in MCP-1 by stimulating fibroblasts, endothelial cells, macrophages and dendritic cells to produce MCP-1 alongside with several other cytokines [24], which might explain remarkably high serum MCP-1 levels in patients with ACD.…”