Imbalance of CD4+CD29+ and CD4+CD45RA+ T-helper cell subsets in peripheral blood of patients with severe atopic dermatitis

Jung, Kwangseon; Bittrich, A; Klimmek, V; Schubert, H.

doi:10.1007/bf01112915

Cited by 8 publications

(3 citation statements)

References 27 publications

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“…We have recently hypothesized that the skin of patients with AD may provide a special microenvironment which either shifts invading T cells toward a Th2-like secretion pattern or leads to preferential homing of Th2-cells into the skin (10). In a previous study, we also have shown a decreased number of UCHL-1-positive "memory" T cells in the peripheral blood of patients with severe AD, suggesting an increased influx of these cells into the skin (11).…”

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confidence: 85%

Adhesion molecules in atopic dermatitis: VCAM-1 and ICAM-1 expression is increased in healthy-appearing skin

Jung

Linse

Heller³

et al. 1996

Allergy

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In the skin of normal and atopic individuals, the expression of E‐selecting (ELAM‐l), L‐selectin (LECAM‐l), P‐selection (CD62), CD31 (PECAM), vascular cell adhesion molecule‐1 (VCAM‐l), intercellular adhesion molecule‐1 (ICAM‐l), and cutaneous lymphocyte antigen (CLA) were compared by immunostaining of skin biopsies which were taken from normal individuals (n= 17), the healthy‐appearing skin of patients with atopic dermatitis (n = lo), and their acute (n = 5) and chronic (n = 6) skin lesions. In contrast to ELAM‐1, the expression of VCAM‐1 and ICAM‐1 was found to be significantly increased in non lesional atopic skin in comparison to the skin of normal individuals. Moreover, in contrast to normal skin of healthy individuals, nonlesional atopic skin showed a further increase of VCAM‐1, ICAM‐1, and ELAM‐1 when cultured with medium alone. This suggests that certain adhesion molecules are constitutively upregulated in healthy‐appearing skin of patients with atopic dermatitis. In addition, atopic skin appears to respond to nonspecific stimuli (such as culture with medium alone) with upregulation of VCAM‐1, ICAM‐1, and ELAM‐1. It is suggested that the observed upregulation of adhesion molecules is mediated by the release of cytokines such as interleukin‐4 from cells which reside in atopic skin. The question of whether the inherent up regulation of adhesion molecules in atopic skin contributes to the development of Th2 cells, which have been found to predominate in atopic inflammation, has to be further investigated.

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confidence: 85%

Adhesion molecules in atopic dermatitis: VCAM-1 and ICAM-1 expression is increased in healthy-appearing skin

Jung

Linse

Heller³

et al. 1996

Allergy

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“…21 This defect in an over abundance of resting T cells defined with CD45RA (formerly 2H4 + ) was not restricted to T1D but extends broadly in autoimmune diseases such as autoimmune atopic dermatitis and inflammatory bowel disease. 22,23 CD45RA resting T cells were originally called T4 + 2H4 + cells (naïve cells) and CD45RO activated cells were originally called T4 + 4B4 cells (memory cells) before the standardization with CD markers. When examining all peripheral T cells, T1D subjects have an abundance of resting CD45RA T cells with poor in vivo conversion to activated CD45RO expressing T lymphocytes.…”

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confidence: 99%

Treg activation defect in type 1 diabetes: correction with TNFR2 agonism

et al. 2016

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Activated T-regulatory cells (aTregs) prevent or halt various forms of autoimmunity. We show that type 1 diabetics (T1D) have a Treg activation defect through an increase in resting Tregs (rTregs, CD4+CD25+Foxp3+CD45RA) and decrease in aTregs (CD4+CD25+Foxp3+CD45RO) (n= 55 T1D, n=45 controls, P=0.01). The activation defect persists life long in T1D subjects (T1D=45, controls=45, P=0.01, P=0.04). Lower numbers of aTregs had clinical significance because they were associated with a trend for less residual C-peptide secretion from the pancreas (P=0.08), and poorer HbA1C control (P=0.03). In humans, the tumor necrosis factor receptor 2 (TNFR2) is obligatory for Treg induction, maintenance and expansion of aTregs. TNFR2 agonism is a method for stimulating Treg conversion from resting to activated. Using two separate in vitro expansion protocols, TNFR2 agonism corrected the T1D activation defect by triggering conversion of rTregs into aTregs (n=54 T1D, P<0.001). TNFR2 agonism was superior to standard protocols and TNF in proliferating Tregs. In T1D, TNFR2 agonist-expanded Tregs were homogeneous and functionally potent by virtue of suppressing autologous cytotoxic T cells in a dose-dependent manner comparable to controls. Targeting the TNFR2 receptor for Treg expansion in vitro demonstrates a means to correct the activation defect in T1D.

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“…With regard to the number of memory cells in the peripheral blood of patients with atopic dermatitis, there have been reports of either no change or a significant decrease compared with healthy controls [11,36]. Furthermore, in atopic patients, the number of memory cells in blood has been found to be diminished in cases with severe atopic dermatitis, but not in those with mild or moderate disease [23].…”

Section: Discussionmentioning

confidence: 95%

Immunophenotyping of the cellular infiltrate in the early elicitation phase of contact dermatitis in the skin of presensitized atopic individuals

Garmann

Gollnick

1995

Arch Dermatol Res

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Little is known about the composition of the cellular infiltrate in the early elicitation phase of contact allergy in atopic individuals. Therefore, we rechallenged ten presensitized disease-free atopic volunteers with their known contact allergen and performed biopsies at time 0 and after 6 and 24 h. Ten patients with acute exacerbated atopic dermatitis in the early stage were chosen as a control group. Skin biopsy specimens were processed for immunohistochemistry (APAAP) and evaluated by computer-assisted morphometry. CD4+ and CD45R0+ cells were found to be significantly increased after 6 (t6) and 24 h (t24), and this was accompanied by an enhanced TCR alpha/beta receptor expression at t6-CD45O+ cells showed a marked influx into the epidermis at t24. CD8+ cells infiltrated the basal layer of the epidermis, thus changing the CD4/CD8 ratio from 4.6:1 at t0 to 2.2:1 at t6. CD1a+ epidermal dendritic cells increased significantly from 811 +/- 240/mm2 at t0, to 1210 +/- 333/mm2 at t24 (P < 0.01). At t6 and t24, a so-called 'epitope CD1a+ shedding' was observed into the intercellular spaces of keratinocytes as well as an elongation and enlargement of the dendrites of CD1a+ cells. In the upper dermis, the number of CD1a+ cells increased from 1098 +/- 485/mm2 at t0 to 2388 +/- 740/mm2 at t24 (P < 0.01). In 7/10 volunteers, IgE+ dendritic cells increased significantly in number at t6 (P < 0.02). The activation markers HLA-DR and CD25 were expressed most distinctly at t24. Interestingly, expression of ICAM-1 on keratinocytes occurred only in four of the ten atopic volunteers.(ABSTRACT TRUNCATED AT 250 WORDS)

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Imbalance of CD4+CD29+ and CD4+CD45RA+ T-helper cell subsets in peripheral blood of patients with severe atopic dermatitis

Cited by 8 publications

References 27 publications

Adhesion molecules in atopic dermatitis: VCAM-1 and ICAM-1 expression is increased in healthy-appearing skin

Adhesion molecules in atopic dermatitis: VCAM-1 and ICAM-1 expression is increased in healthy-appearing skin

Treg activation defect in type 1 diabetes: correction with TNFR2 agonism

Immunophenotyping of the cellular infiltrate in the early elicitation phase of contact dermatitis in the skin of presensitized atopic individuals

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