Early inflammatory markers in elicitation of allergic contact dermatitis

Martín, Andrea P.; Gallino, Norberto; Gagliardi, Julio; Ortiz, Susana; Lascano, Alejandro Ruíz; Diller, Ana; Daraio, María Cristina; Kahn, Adrian M.; Mariani, Ana Lía; Serra, Horacio M.

doi:10.1186/1471-5945-2-9

Cited by 13 publications

(12 citation statements)

References 47 publications

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“…As we have shown previously, the skin biopsies from positive reactions showed signs of hypertrophy and swelling of BECs as well as expression of CS-1 fibronectin and CCL17 starting at 2 and 10 h, respectively [21](table 1). A typical Th1/Tc1 immune response was observed, since the majority of mononuclear cells around dermal BECs expressed the chemokine receptor CXCR3 (mean 63.5% in the positive antigen-challenged site versus 6.3% in the control skin).…”

Section: Resultsmentioning

confidence: 88%

“…We investigated the kinetics of CCL21 expression in skin from patients with ACD, a disease in which the sensitization phase is strongly dependent on LC migration, and where expression of important ligands for integrins and chemokine receptors plays a key role in the skin homing of effector Th1/Tc1 lymphocytes [21, 26, 27]. In this regard, we corroborated our previous finding of early expression on BECs of CS-1 fibronectin and TARC, which was followed by a progressive and significant accumulation of CXCR3+ cells in the positive patch test biopsies, clearly indicating the involvement of a Th1/Tc1 immune response.…”

Section: Discussionmentioning

confidence: 99%

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Secondary Lymphoid Tissue Chemokine (CCL21) Is Upregulated in Allergic Contact Dermatitis

Serra

Eberhard²,

Martín³

et al. 2004

Int Arch Allergy Immunol

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Chemokines are important players in the development of allergic contact dermatitis (ACD). The participation of secondary lymphoid tissue chemokine (CCL21) is essential in the induction of the disease due to its expression in lymphatic vessels and in secondary lymphoid organs. Since there is no information about its participation during the effector phase of ACD, we studied this chemokine in patients already diagnosed with ACD, who were challenged with the relevant positive and negative (control) antigens. All patients showed a specific antigen-induced immune response characterized by early expression of inflammatory markers in blood endothelial cells followed by dermal accumulation of mononuclear cells with an important increase in infiltration of CXCR3+ but not of CCR7+ cells. In situ hybridization and immunohistochemistry showed low levels of CCL21 in lymphatic vessels at 2 h, whereas they were significantly increased at 10 and 48 h in all positive patch tests. In contrast, very low expression of this chemokine was observed in skin biopsies from the control site at 48 h. In addition, Langerin+ cells, which were present in dermis from positive patch tests at 2 h, were diminished in number at 10 and 48 h, but a significant number of those cells was still present in dermal areas of the control site at 48 h. We demonstrate for the first time that CCL21, a constitutively expressed chemokine, is strongly upregulated in human lymphatic vessels during a Th1/Tc1 allergic inflammatory response. This can provide the signal required for CCR7+ cells to leave the skin through CCL21-positive lymphatic vessels.

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Section: Resultsmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Secondary Lymphoid Tissue Chemokine (CCL21) Is Upregulated in Allergic Contact Dermatitis

Serra

Eberhard²,

Martín³

et al. 2004

Int Arch Allergy Immunol

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“…Activated T cells release proinflammatory cytokines, which then activate local tissue cells, leading to the characteristic late effector responses at 24-48 hours (16-18). In the elicitation phase, the main effector cells have been demonstrated to be IFN-γ-producing CD8 + Tc1 cells (19-21). Thus, CHS is a prototypic T cell-mediated response.…”

Section: Introductionmentioning

confidence: 99%

CD22 Expression Mediates the Regulatory Functions of Peritoneal B-1a Cells during the Remission Phase of Contact Hypersensitivity Reactions

Nakashima

Hamaguchi

Watanabe

et al. 2010

The Journal of Immunology

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While contact hypersensitivity (CHS) has been considered a prototype of T cell-mediated immune reactions, recently a significant contribution of regulatory B cell subsets in the suppression of CHS has been demonstrated. CD22, one of the Siglecs, is a B cell-specific molecule that negatively regulates B cell receptor signaling. To clarify the roles of B cells in CHS, CHS in CD22-/- mice was investigated. CD22-/- mice showed delayed recovery from CHS reactions compared with wild type mice. Transfer of wild type peritoneal B-1a cells reversed the prolonged CHS reaction seen in CD22-/- mice, and this was blocked by the simultaneous injection with IL-10 receptor Ab. While CD22-/- peritoneal B-1a cells were capable of producing IL-10 at wild type levels, intraperitoneal injection of differentially labeled wild type/CD22-/- B cells demonstrated that a smaller number of CD22-/- B cells resided in lymphoid organs 5 days after CHS elicitation, suggesting a defect in survival or retention in activated CD22-/- peritoneal B-1 cells. Thus, our current study reveals a regulatory role for peritoneal B-1a cells in CHS. Two distinct regulatory B cell subsets cooperatively inhibit CHS responses. While splenic CD1dhiCD5+ B cells have a crucial role in suppressing the acute exacerbating phase of CHS, peritoneal B-1a cells are likely to suppress the late remission phase as “regulatory B cells”. CD22 deficiency results in disturbed CHS remission by impaired retention or survival of peritoneal B-1a cells that migrate into lymphoid organs.

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“…In the case of asthma the pathogenic role of the CCL17/CCL22-CCR4 axis is still controversial (Pease, 2006), as some reports demonstrate efficient improvement of disease symptoms after CCR4 or CCL17 blockade (Kawasaki et al, 2001;Perros et al, 2009;Vijayanand et al, 2010), whereas others do not ( Chvatchko et al, 2000;Conroy et al, 2003). As already mentioned above, enhanced expression of CCL17 and CCL22 has also been observed in allergic contact dermatitis (Bäumer et al, 2004;Goebeler et al, 2001;Kamsteeg et al, 2010;Martín et al, 2002), and contact hypersensitivity responses were significantly inhibited in CCL17-deficient mice (Alferink et al, 2003). Regarding nonallergic diseases, CCL17 has recently been shown to enhance the formation of artherosclerotic lesions in mice by inhibition of Treg cell expansion (Weber et al, 2011).…”

Section: Implication Of Ccl17 Ccl22 and Ccr4 In Other Diseasesmentioning

confidence: 72%

“…A possible link between skin barrier dysfunction and CCL17 was recently reported by Nakahigashi et al, who showed that CCL17 was able to induce aquaporin-3 in human keratinocytes, which in turn promoted keratinocyte proliferation and disturbed barrier function (Nakahigashi et al, 2010). Whereas elevated levels of CCL17 and CCL22 have also been observed in allergic contact dermatitis (Bäumer et al, 2004;Goebeler et al, 2001;Kamsteeg et al, 2010;Martín et al, 2002;), CCL17/CCL22 expression is not significantly increased in Psoriasis vulgaris (Gros et al, 2009;Kakinuma et al, 2002;Kamsteeg et al, 2010;Uchida et al, 2002). This correlates with the fact that psoriasis is a Th1 dominated disease, whereas Th2-type cytokines and chemokines dominate the initial phase of AD, with a shift to Th1-type cytokines in the chronic phase (Grewe et al, 1998;Fujita et al, 2011).…”

Section: Ccl17 As a Biomarker For Disease Severity In Admentioning

confidence: 98%