Increased T-cell receptor Vβ2 chain expression in skin homing lymphocytes in psoriasis

Davison, S C; Allen, Michael; Harmer, A.; Vaughan, R. W.; Barker, Jonathan

doi:10.1046/j.1365-2133.1999.02813.x

Cited by 15 publications

(12 citation statements)

References 17 publications

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“…Furthermore, we noticed that more CLA ϩ T cells could be detected within PBMCs of psoratic vs normal donors (Table I). This observation parallels recent findings of Davison et al (42).…”

Section: Skin Homing Cla ϩ T Cells Of Psoriatic Patients Respond To Lsupporting

confidence: 80%

Up-Regulation of Macrophage Inflammatory Protein-3α/CCL20 and CC Chemokine Receptor 6 in Psoriasis

Homey¹,

Dieu-Nosjean²,

Wiesenborn

et al. 2000

The Journal of Immunology

508

412

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Autoimmunity plays a key role in the immunopathogenesis of psoriasis; however, little is known about the recruitment of pathogenic cells to skin lesions. We report here that the CC chemokine, macrophage inflammatory protein-3α, recently renamed CCL20, and its receptor CCR6 are markedly up-regulated in psoriasis. CCL20-expressing keratinocytes colocalize with skin-infiltrating T cells in lesional psoriatic skin. PBMCs derived from psoriatic patients show significantly increased CCR6 mRNA levels. Moreover, skin-homing CLA+ memory T cells express high levels of surface CCR6. Furthermore, the expression of CCR6 mRNA is 100- to 1000-fold higher on sorted CLA+ memory T cells than other chemokine receptors, including CXCR1, CXCR2, CXCR3, CCR2, CCR3, and CCR5. In vitro, CCL20 attracted skin-homing CLA+ T cells of both normal and psoriatic donors; however, psoriatic lymphocytes responded to lower concentrations of chemokine and showed higher chemotactic responses. Using ELISA as well as real-time quantitative PCR, we show that cultured primary keratinocytes, dermal fibroblasts, and dermal microvascular endothelial and dendritic cells are major sources of CCL20, and that the expression of this chemokine can be induced by proinflammatory mediators such as TNF-α/IL-1β, CD40 ligand, IFN-γ, or IL-17. Taken together, these findings strongly suggest that CCL20/CCR6 may play a role in the recruitment of T cells to lesional psoriatic skin.

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“…Furthermore, we noticed that more CLA ϩ T cells could be detected within PBMCs of psoratic vs normal donors (Table I). This observation parallels recent findings of Davison et al (42).…”

Section: Skin Homing Cla ϩ T Cells Of Psoriatic Patients Respond To Lsupporting

confidence: 80%

Up-Regulation of Macrophage Inflammatory Protein-3α/CCL20 and CC Chemokine Receptor 6 in Psoriasis

Homey¹,

Dieu-Nosjean²,

Wiesenborn

et al. 2000

The Journal of Immunology

508

412

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“…Davison et al. 6 demonstrated an increase in the number of circulating TCRβV2 (IMGT TCRβV20) T cells in psoriatic patients, relative to controls. They concluded that these cells were homing to the skin under the influence of an antigen‐driven selection 6 .…”

mentioning

confidence: 99%

“…They concluded that these cells were homing to the skin under the influence of an antigen-driven selection. 6 Tassiulas et al 7 demonstrated TCRbV expansions common to both skin and synovium in nine patients with psoriatic arthropathy. In one patient they demonstrated a clone shared between the skin and the synovium, suggesting an antigen shared at both sites.…”

mentioning

confidence: 99%

T-cell receptor repertoire in pyoderma gangrenosum: evidence for clonal expansions and trafficking

et al. 2007

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Background The cause of pyoderma gangrenosum (PG) is unknown, but it is likely to be an immune-mediated disease because it is often associated with conditions such as inflammatory bowel disease and rheumatoid arthritis. T cells play an important role in these conditions and have been implicated in the pathogenesis of other skin diseases such as psoriasis.Objectives We examined the T-cell receptor repertoire in PG in order to test the hypothesis that if the T cells were responding to antigen, there would be expanded T-cell clones in the skin and the circulation of these patients. Patients and methods We studied five patients with PG and examined the T-cell receptor repertoire in cells taken from the peripheral blood and from biopsies of the ulcers, using complementarity determining region 3 spectratyping. Results We were able to demonstrate expanded clones in the peripheral blood lymphocyte population of each patient. Clonal expansions within the skin were found in four of the five patients. Most significantly, expanded clones that were shared between the blood and the skin were revealed in four of the five patients.Conclusions These findings imply that T cells play an integral role in the development of PG and suggest that T cells are trafficking to the skin under the influence of an antigenic stimulus.

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“…Davison et al [35] described increased expression of BV2 in CLA+ psoriatic peripheral blood-derived T cells. Preferential usage of certain BV families suggests superantigen involvement in psoriasis.…”

Section: Studies In Psoriasismentioning

confidence: 98%

Disease Mechanisms in psoriasis and psoriatic arthritis

Costello¹,

FitzGerald

2001

Curr Rheumatol Rep

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Any hypothesis that tries to explain disease mechanisms in psoriasis and psoriatic arthritis (PsA) must take into account the containment of the inflammatory process to three specific sites: the skin, synovium, and enthesis. This article reviews the recent literature that advances our understanding of disease mechanisms at these specific sites. Additional progress will be achieved by research that focuses on common pathogenic pathways at these sites, in particular when searching for foreign candidates or auto-antigens triggering the T-cell-mediated immune response.

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Increased T-cell receptor Vβ2 chain expression in skin homing lymphocytes in psoriasis

Cited by 15 publications

References 17 publications

Up-Regulation of Macrophage Inflammatory Protein-3α/CCL20 and CC Chemokine Receptor 6 in Psoriasis

Up-Regulation of Macrophage Inflammatory Protein-3α/CCL20 and CC Chemokine Receptor 6 in Psoriasis

T-cell receptor repertoire in pyoderma gangrenosum: evidence for clonal expansions and trafficking

Disease Mechanisms in psoriasis and psoriatic arthritis

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