Immunophenotyping of the Cutaneous Infiltrate and of the Mononuclear Cells in the Peripheral Blood in Patients With Atopic Dermatitis

Lever, Rosemary; Turbitt, Marlyn L.; Sanderson, Andrew; MacKie, Rona M.

doi:10.1111/1523-1747.ep12579727

Cited by 76 publications

(24 citation statements)

References 32 publications

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“…Our observation that the predominance of helper-inducer lymphocytes is a general feature of chronic inflammatory infiltrates has been confirmed in a variety of pathological situations, for example in thyroid tissue in Grave's disease [23] and in atopic dermatitis [24]. It is apparent that many of the immunological properties of lymphocytes from inflammatory infiltrates, such as the synovium, can be explained in terms of their predominantly helper-inducer phenotype (Table 1).…”

Section: Discussionsupporting

confidence: 60%

The preferential accumulation of helper‐inducer T lymphocytes in inflammatory lesions: evidence for regulation by selective endothelial and homotypic adhesion

et al. 1988

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The mechanisms which lead to the accumulation of T lymphocytes into inflammatory lesions are not clearly understood. We have previously shown that synovial CD4 T lymphocytes are mostly CDw29+UCHL1+ (helper-inducer cells) and very few carry the CD45R antigen which identifies the suppressor-inducer subset. Synovial CD8+ cells are also CDw29+UCHL1+CD45R-. In the present study, lymphocytes from pleural and peritoneal inflammatory infiltrates were shown to have a similar phenotypic pattern. Furthermore, it was demonstrated that the CDw29+UCHL1+ subset had a greater ability than CD45R+ cells to adhere to endothelial cells and to form homotypic clusters. Differential surface expression of LFA-1 on the two subsets was also shown, but this could not account for the demonstrated adhesion differences. Differences in adhesion between CDw29+/UCHL1+ and CD45R+ cells may explain the preferential accumulation of CDw29+/UCHL1+ cells in inflammatory infiltrates and underlie some of the functional differences between cells taken from sites of chronic inflammation and those from peripheral blood.

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Section: Discussionsupporting

confidence: 60%

The preferential accumulation of helper‐inducer T lymphocytes in inflammatory lesions: evidence for regulation by selective endothelial and homotypic adhesion

et al. 1988

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“…At an earlier time point, our in situ results approximately correlate to the in vitro results from Werfel et al [28 ]showing a proportion of 10–15% CD8+ allergen-specific T cells from lesional AE skin. Our results confirm previous reports [29, 30] demonstrating that more inflammatory cells are present in non-lesional AE skin compared to non-atopic skin, albeit in far smaller amounts than in lesional AE skin.…”

Section: Discussionsupporting

confidence: 93%

Pollen Grains Induce a Rapid and Biphasic Eczematous Immune Response in Atopic Eczema Patients

Eyerich

Huss‐Marp

Darsow

et al. 2007

Int Arch Allergy Immunol

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Introduction: Eczematous reactions to type I allergy-inducing antigens are documented in a subgroup of patients with atopic eczema. Yet, the underlying immunological mechanisms are not well understood. Material and Methods: To delineate the effect of native pollen grains on human skin of healthy and atopic individuals we performed patch tests (atopy patch test with native pollen grains, PPT). Nickel patch tests (NPT) served as an established model of contact dermatitis. Skin site biopsies were taken 6–96 h after allergen application and investigated immunohistochemically. Results: Histology of positive patch tests showed an influx of mononuclear cells (predominantly CD4+, CD25+, CD45RO+). This influx was detected earlier in the PPT reaction than in the immune response to nickel. A biphasic cytokine response could be detected in the PPT: IL-5 dominated in the early, IFN-γ in the late phase. The NPT was continuously dominated by IFN-γ. Dendritic cell subpopulations imitated the earlier kinetics of the mononuclear infiltrate. Discussion: Thus, pollen grains induce eczematous reactions in susceptible individuals. This reaction appears clinically and immunohistochemically similar to the contact hypersensitivity reaction to nickel but follows a faster kinetic and a biphasic course: Th2 and IgE in the early (24 h) and Th1 predominance in the late (96 h) phase.

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“…We have considered that such freshly prepared, resting peripheral blood T cells are not representative of the populations of extravascular effector cells that will encounter immobilized ECMP and that are involved in the pathogenesis of inflammatory and autoimmune diseases. For example, in the skin lesions of atopic dermatitis, essentially all dermal T cells were found strongly to express the activation marker, HLA-DR, whereas less than 4% of peripheral blood T cells were HLA-DR ϩ (28). Similarly, in the skin lesions of psoriasis, more than 80% of dermal CD4 ϩ T cells were HLA-DR ϩ (29).…”

mentioning

confidence: 99%

Potent Costimulation of Effector T Lymphocytes by Human Collagen Type I

Rao

Hales

Camp

2000

The Journal of Immunology

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Purified, resting peripheral blood T lymphocytes were previously reported to undergo β1 integrin-dependent activation when cultured with anti-CD3 mAb coimmobilized with fibronectin, but not type I collagen. However, the extravascular T cells that encounter immobilized extracellular matrix proteins and are involved in disease pathogenesis have different properties from resting peripheral blood cells. In this study, we confirm that resting CD4+ and CD8+ T cells from peripheral blood are costimulated by immobilized fibronectin, but not type I collagen. In contrast, Ag- or mitogen-stimulated CD4+ and CD8+ T cell lines, used as models of the effector cells involved in disease, are more potently costimulated by type I collagen than fibronectin. The collagen-induced effects are similar in assays with serum-free medium and in more physiological assays in which anti-CD3 mAb is replaced by a threshold concentration of Ag and irradiated autologous PBMC as APC. The responses are β1 integrin dependent and mediated largely by very late Ag (VLA) 1 and 2, as shown by their up-regulation on the T cell lines as compared with freshly purified resting PBL, and by the effects of blocking mAb. Reversed phase HPLC located the major costimulatory sequence(s) in the α1 chain of type I collagen, the structure of which was confirmed by amino acid sequencing. The results demonstrate the potential importance of type I collagen, an abundant extracellular matrix protein, in enhancing the activation of extravascular effector T cells in inflammatory disease, and point to a new immunotherapeutic target.

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Immunophenotyping of the Cutaneous Infiltrate and of the Mononuclear Cells in the Peripheral Blood in Patients With Atopic Dermatitis

Cited by 76 publications

References 32 publications

The preferential accumulation of helper‐inducer T lymphocytes in inflammatory lesions: evidence for regulation by selective endothelial and homotypic adhesion

The preferential accumulation of helper‐inducer T lymphocytes in inflammatory lesions: evidence for regulation by selective endothelial and homotypic adhesion

Pollen Grains Induce a Rapid and Biphasic Eczematous Immune Response in Atopic Eczema Patients

Potent Costimulation of Effector T Lymphocytes by Human Collagen Type I

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