Early migration of cutaneous lymphocyte‐associated antigen (CLA) positive T cells into evolving psoriatic plaques

Davison, S C; Ballsdon, A. E.; Allen, Michael; Barker, Jonathan

doi:10.1034/j.1600-0625.2001.100408.x

Cited by 51 publications

(50 citation statements)

References 20 publications

(16 reference statements)

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“…Following ethical approval and informed consent, paired biopsies were taken from lesional skin and clinically normal, nonlesional skin, 1 cm in advance of the active edge of the lesion, as identified by laser Doppler fluxmetry (Davison et al, 2001) in adult psoriatic patients (n ϭ 17). Biopsies were also taken from normal volunteers (n ϭ 6).…”

Section: Immunohistochemistrymentioning

confidence: 99%

Corneodesmosin Expression in Psoriasis Vulgaris Differs from Normal Skin and Other Inflammatory Skin Disorders

Allen

Ishida‐Yamamoto

McGrath

et al. 2001

Laboratory Investigation

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SUMMARY:Corneodesmosin (Cdsn) is a late differentiation epidermal glycoprotein putatively involved in keratinocyte adhesion.The Cdsn gene lies within the susceptibility region on chromosome 6p21.3 (PSORS1) for psoriasis, a common chronic disfiguring skin disease. A particular allelic variant of Cdsn has a strong association with psoriasis. Therefore, genetically and biologically, Cdsn is a possible candidate gene for psoriasis susceptibility. To investigate a potential role for Cdsn in psoriasis pathogenesis, protein expression studies were performed by quantitative immunohistochemistry on normal skin, psoriatic skin (lesional and nonlesional), and other skin disorders using monoclonal antibodies (G36-19 and F28-27). In normal and nonlesional skin, Cdsn was expressed in stratum corneum and one or two layers of superficial stratum granulosum. In lesional psoriasis, there was a significant increase in Cdsn expression, which was observed in multiple layers of stratum spinosum and in stratum corneum. The expression pattern varied from granular, cytoplasmic immunoreactivity to cell surface labeling with weakly immunoreactive cytoplasm. In chronic atopic dermatitis, lichen planus, mycosis fungoides, and pityriasis rubra pilaris, Cdsn immunoreactivity was confined to stratum corneum and upper stratum granulosum with no stratum spinosum immunoreactivity. Immunoelectron microscopy of normal and lesional psoriatic skin demonstrated Cdsn release concomitant with involucrin incorporation into cell envelopes and completed before mature envelope formation. Extracellular release of Cdsn occurred at a lower level of the epidermis in psoriasis than normal skin. These protein expression studies provide evidence of altered Cdsn expression in psoriasis consistent with a role of Cdsn in disease pathogenesis. Further functional and genetic studies of Cdsn are justified to determine its role as a potential psoriasis-susceptibility factor. (Lab Invest 2001, 81:969 -976).

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Section: Immunohistochemistrymentioning

confidence: 99%

Corneodesmosin Expression in Psoriasis Vulgaris Differs from Normal Skin and Other Inflammatory Skin Disorders

Allen

Ishida‐Yamamoto

McGrath

et al. 2001

Laboratory Investigation

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“…This conclusion was based on the observation that cytokine levels were highly impaired after blocking HLA class I and class II molecules. Interestingly, if circulating CLA+ T cells were cocultured with nonlesional epidermal cells, levels of several inlammatory mediators were upregulated when cells were activated with S. pyogenes, thus supporting the initial role of CLA+ T cells in driving nonlesional skin to the plaque formation [42,43].Overall, this novel model provided irst evidence of a direct implication of CLA+ T cells and S. pyogenes in psoriasis samples treated ex vivo, while no such response was reproduced with healthy samples. These irst results shed new light on the study of psoriasis, providing a tool for further valuable translational studies.…”

mentioning

confidence: 74%

Human Translational Research in Psoriasis Using CLA+ T Cells

Ruiz-Romeu¹,

Santamaria‐Babí²

2017

An Interdisciplinary Approach to Psoriasis

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Focusing on the study of human memory CLA+ T cells to understand psoriasis pathology constitutes an innovative approach to explore the pathological mechanism of this chronic cutaneous inlammatory disease. CLA+ T cells can be considered peripheral cell biomarkers in the study of T-cell mediated human skin diseases. During the last few years, new evidences have been found that link streptococcal infection with IL-17 response in psoriasis by studying the interaction between Streptococcus pyogenes with CLA+ T cells and autologous epidermal cells. S. pyogenes constitutes the best clinically characterized trigger of psoriasis and by exploring its efect on CLA+ T cells and epidermal cells in psoriasis may allow understanding psoriasis by using patient's clinical samples ex vivo. Keywords: psoriasis, CLA+ T cells, translational research, Streptococcus pyogenes, IL17 CLA+ T cells and the regional cutaneous immune systemThe adaptive immune responses taking place during cutaneous chronic inlammation in psoriasis preferentially involve a subset of memory T lymphocytes, which are related to the skin and that belong to the cutaneous immune system, and constitute one of the best characterized regional immune systems of the body and known for decades [1]. In the humans, the cutaneous lymphocyte-associated antigen (CLA) is a surface cell marker that allows identifying T cells that belong to the cutaneous immune system. The CLA antigen is a carbohydrate expressed by 15% of human circulating T cells, and on most (>90%) skin-iniltrating T cells, contrary to other inlamed organs [2]. CLA is expressed preferentially on memory antigenexperienced T cells.© 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.The CLA is one of the adhesion molecule that, together with chemokine receptors, allows T cells to selectively migrate to the skin, in either homeostatic or inlammatory conditions, by binding to endothelial cell wall via adhesion molecules or ligands. The molecular interactions between CLA/E-selectin, very late antigen-4 (VLA-4)/vascular cell adhesion protein-1 (VCAM-1), lymphocyte function-associated antigen-1 (LFA-1)/intercellular adhesion molecule-1 (ICAM-1), and chemokine ligands for chemokine, C-C motif receptor (CCR) 10, CCR4, CCR6, and CCR8 constitute a code bar system enabling skin iniltration [3].The importance of circulating CLA+ T cells for understanding the skin immune system is not only based on their capacity to selectively migrate to skin, but also on the fact that these circulating memory T cells are functionally related to the immune response taking place in the cutaneous inlamed lesions. This feature is based on the recirculating capacity of those cells between lesional skin and blood during cutaneous inlammation in psoriasis [3]. The adhesive interaction between LFA-1 ...

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“…The majority of T cells in psoriasis skin lesions express CLA (36), and the dermal venules express P-selectin (37). CHO-131 reactivity was also evident in psoriatic lesions, which primarily colocalized with CD3 staining (Fig.…”

Section: Enrichment Of Cho-131 ϩ T Cells In Psoriatic Skin Lesionsmentioning

confidence: 93%

“…It is possible that CHO-131 ϩ T cell accumulation in psoriatic lesions results from the induction of C2-O-sLe X expression by re-stimulated T cells, which remains to be determined. However, it has been shown that CLA ϩ T cell accumulation occurs in conjunction with evolving skin lesions rather than as an acquisition of this phenotype following T cell migration into skin (36).…”

Section: Enrichment Of Cho-131 ϩ T Cells In Psoriatic Skin Lesionsmentioning

confidence: 99%

The Monoclonal Antibody CHO-131 Identifies a Subset of Cutaneous Lymphocyte-Associated Antigen T Cells Enriched in P-Selectin-Binding Cells

Campbell

Niehans

et al. 2006

The Journal of Immunology

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T cells use the vascular adhesion molecules E- and P-selectin to enter inflamed skin. Previous studies have indicated the possibility for diversity in the synthesis of E- and P-selectin glycan ligands by activated T cells due to their different requirements for the O-glycan branching enzyme core 2 β1,6-N-acetylglucosaminyltransferase I and its independent regulation. It is known that T cell staining by the mAb HECA-452 (referred to as cutaneous lymphocyte-associated Ag (CLA) T cells) correlates with E-selectin binding, yet whether these cells uniformly bind P-selectin is less clear. The mAb CHO-131 and P-selectin binding require a glycan moiety consisting of a sialylated and fucosylated oligosaccharide properly positioned on a core-2 O-glycan. Interestingly, CHO-131 stains a subset of CLA+ T cells. A direct comparison of the selectin binding capacity of CHO-131+ and CHO-131− CLA+ T cells revealed a significantly greater P-selectin, but not E-selectin, binding activity by the former subset. Based on the expression of homing and central and effector memory cell markers, CHO-131+ and CHO-131− CLA+ T cells have an overlapping skin-tropic and memory phenotype. CHO-131+ T cells were considerably enriched in psoriatic skin, yet, unlike the peripheral blood of healthy individuals, HECA-452 and CHO-131 stained a similar proportion of T cells in the cutaneous lesions, indicating an accumulation advantage by CHO-131+ T cells. We conclude that the CHO-131+CLA+ T cell subset is enriched in P-selectin binding cells. These findings should provide new insights into the regulation and function of skin homing T cells.

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Early migration of cutaneous lymphocyte‐associated antigen (CLA) positive T cells into evolving psoriatic plaques

Cited by 51 publications

References 20 publications

Corneodesmosin Expression in Psoriasis Vulgaris Differs from Normal Skin and Other Inflammatory Skin Disorders

Corneodesmosin Expression in Psoriasis Vulgaris Differs from Normal Skin and Other Inflammatory Skin Disorders

Human Translational Research in Psoriasis Using CLA+ T Cells

The Monoclonal Antibody CHO-131 Identifies a Subset of Cutaneous Lymphocyte-Associated Antigen T Cells Enriched in P-Selectin-Binding Cells

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