CD7-Negative Helper T Cells Accumulate in Inflammatory Skin Lesions

Moll, Martina; Reinhold, Uwe; Kukel, Sylvia; Abken, Hinrich; Müller, Rainer H.; Oltermann, Iris; Kreysel, H. W.

doi:10.1111/1523-1747.ep12371791

Cited by 71 publications

(56 citation statements)

References 20 publications

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“…Sezary cells which are pathognomic for the leukemic variant of the cutaneous T cell lymphoma mycosis fungoides are typically CD7 Ϫ (20). CD7 Ϫ CD4 ϩ T cells also represent a major subpopulation of the infiltrates in inflammatory skin diseases suggesting that these cells tend to accumulate at inflammatory sites (21).…”

Section: Cd4mentioning

confidence: 99%

CD4+ CD7- CD28- T cells are expanded in rheumatoid arthritis and are characterized by autoreactivity.

Goronzy²,

1996

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Clonal expansion of CD4ϩ T cells is a characteristic finding in patients with RA and is only infrequently found in patients with psoriatic arthritis and healthy controls. Expanded CD4ϩ clonotypes are present in the blood, infiltrate into the joint, and persist over years. We have now addressed the question of whether the expanded clonotypes have unique functional and phenotypic properties which may explain the preferential in vivo expansion in RA. In contrast to most CD4 ϩ T cells, expanded clonotypes lacked the expression of the CD28 and CD7 cell surface molecules. Accordingly, the subsets of CD4 ϩ CD28 Ϫ (9.7 vs. 1.7, P ϭ 0.00002) and CD4 ϩ CD7 Ϫ T cells (21.5 vs. 12.6, P ϭ 0.018) were increased in RA patients compared with age-matched normal individuals. Despite the lack of CD28 expression, clonally expanded CD4 ϩ T cells were not anergic but proliferated in response to immobilized anti-CD3 and could be maintained in tissue culture. In vivo expanded CD4 ϩ T cells were autoreactive to ubiquitously distributed autoantigens. They responded in an autologous mixed lymphocyte reaction, and T cell clones isolated from selected patients proliferated to autologous peripheral blood adherent cells. These data suggest that in RA patients selected CD4 ϩ T cells which share the CD7 Ϫ CD28 Ϫ phenotype escape from peripheral tolerance. ( J. Clin. Invest. 1996. 97

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Section: Cd4mentioning

confidence: 99%

CD4+ CD7- CD28- T cells are expanded in rheumatoid arthritis and are characterized by autoreactivity.

Goronzy²,

1996

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“…In contrast to the CD4 + CD7 + T-cell population, CD4 + CD7 7 T cells expand during certain physiological and pathological conditions in vivo. For instance, circulating CD4 + CD7 7 T cells in the peripheral blood increase in both percentages and absolute numbers during aging 1 ± 3 and, furthermore, under conditions that are associated with permanent T-cell stimulation such as chronic inflammatory skin diseases, 4 rheumatoid arthritis, 5,6 and kidney transplantation recipients. 7 We moreover found that preferentially CD4 + CD7 7 T cells infiltrate the skin in diseases associated with chronic immunostimulation.…”

Section: Introductionmentioning

confidence: 99%

The CD7− subset of CD4+ memory T cells is prone to accelerated apoptosis that is prevented by interleukin-15 (IL-15)

et al. 2001

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“…Within the skin, highly increased numbers of CD7 Ϫ T cells are present among lymphocytes cultured from biopsies of inflammatory skin lesions (26) as well as the cutaneous T cell lymphoma, underlining the important role of CD7 during inflammatory processes and malignancies (47). We now expand the role of CD4 ϩ CD7 Ϫ memory T cells by demonstrating that this regulatory T cell type is increased also in CrD and UC tissue, involving these new cell subsets into the complex pathophysiology of IBD.…”

Section: Cd25mentioning

confidence: 72%

“…Modulation of CD7 is associated with an inhibition of T cell proliferation (25) and CD7-negative T cells represent a constant proportion of CD4 ϩ CD45RA Ϫ CD45R0 ϩ memory T cells that accumulate in inflammatory skin lesions (26,27), cutaneous T cell lymphoma, and in the peripheral blood of patients with rheumatoid arthritis (28). Furthermore, CD4 ϩ cells that lack the CD7 Ag express the homing receptor cutaneous lymphocyte Ag (29), preferentially attach to vascular endothelial cells, and accumulate in the skin during chronic inflammation (30).…”

Section: Enhanced Accumulation Of Cd4 ϩ Cd7 ϫ T Cells In Ibdmentioning

confidence: 99%

Proteomic Analysis of the Inflamed Intestinal Mucosa Reveals Distinctive Immune Response Profiles in Crohn’s Disease and Ulcerative Colitis

Berndt

Bartsch²,

Philipsen³

et al. 2007

The Journal of Immunology

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Although Crohn’s disease (CrD) and ulcerative colitis (UC) share several clinical features, the mechanisms of tissue injury differ. Because the global cellular function depends upon the protein network environment as a whole, we explored changes in the distribution and association of mucosal proteins to define key events involved in disease pathogenesis. Endoscopic biopsies were taken from CrD, UC, and control colonic mucosa, and Multi-Epitope-Ligand-Cartographie immunofluorescence microscopy with 32 different Abs was performed. Multi-Epitope-Ligand-Cartographie is a novel, highly multiplexed robotic imaging technology which allows integrating cell biology and biomathematical tools to visualize dozens of proteins simultaneously in a structurally intact cell or tissue. In CrD, the number of CD3+CD45RA+ naive T cells was markedly increased, but only activated memory, but not naive, T cells expressed decreased levels of Bax, active caspase-3 or -8. In UC, only CD4+ T cells coexpressing NF-κB were caspase-8 and poly(ADP-ribose)-polymerase positive. Furthermore, the number of CD4+CD25+ T cells was elevated only in UC, whereas in CrD and controls, the number of these cells was similar. By using hub analysis, we also identified that the colocalization pattern with NF-κB+ and poly(ADP-ribose)-polymerase+ as base motifs distinguished CrD from UC. High-content proteomic analysis of the intestinal mucosa demonstrated for the first time that different T cell populations within the intestinal mucosa express proteins translating distinct biological functions in each form of inflammatory bowel disease. Thus, topological proteomic analysis may help to unravel the pathogenesis of inflammatory bowel disease by defining distinct immunopathogenic profiles in CrD and UC.

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CD7-Negative Helper T Cells Accumulate in Inflammatory Skin Lesions

Cited by 71 publications

References 20 publications

CD4+ CD7- CD28- T cells are expanded in rheumatoid arthritis and are characterized by autoreactivity.

CD4+ CD7- CD28- T cells are expanded in rheumatoid arthritis and are characterized by autoreactivity.

The CD7− subset of CD4+ memory T cells is prone to accelerated apoptosis that is prevented by interleukin-15 (IL-15)

Proteomic Analysis of the Inflamed Intestinal Mucosa Reveals Distinctive Immune Response Profiles in Crohn’s Disease and Ulcerative Colitis

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