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Updated: Aug 12, 2026

Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture
Published on: April 8, 2016
Functional CD86 (B7-2/B70) is predominantly expressed on Langerhans cells in atopic dermatitis
O Ohki1, H Yokozeki, I Katayama
1Department of Dermatology, Tokyo Medical and Dental University School of Medicine, Japan.
Insights
CD86 is highly expressed on Langerhans cells in atopic dermatitis lesions and significantly inhibits allergen-induced T-cell proliferation, suggesting a key role in the disease pathogenesis.
Area of Science:
- Immunology
- Dermatology
- Cell Biology
Background:
- Atopic dermatitis (AD) involves complex immune dysregulation.
- Langerhans cells (LCs) are key antigen-presenting cells in the skin.
- Co-stimulatory molecules on LCs modulate T-cell responses.
Purpose of the Study:
- To investigate the expression and function of co-stimulatory molecules CD80 and CD86 on LCs in atopic dermatitis.
- To determine the role of these molecules in the pathogenesis of AD.
Main Methods:
- Immunohistochemical analysis of skin lesions from AD patients and controls.
- Double immunostaining to identify LC markers (CD1a).
- Inhibition assays using anti-CD80 and anti-CD86 monoclonal antibodies to assess T-cell proliferation.
Main Results:
- CD86 was detected on LCs in all AD lesional skin samples, while CD80 was present in only 42%.
- CD86 expression was also noted in non-lesional skin and allergen-challenged sites.
- Anti-CD86 antibody significantly inhibited T-cell proliferation stimulated by Dermatophagoides pteronyssinus allergen, more so than anti-CD80.
Conclusions:
- CD86 is significantly upregulated on LCs in atopic dermatitis.
- CD86 on LCs plays a crucial role in mediating T-cell responses in AD pathogenesis.
- Targeting CD86 may offer a therapeutic strategy for atopic dermatitis.
Abstract:
Recently, we reported the functional expression of CD86 on cultured human Langerhans cells derived from normal epidermis. In the present study, we investigated the expression and function of co-stimulatory molecules in the pathogenesis of atopic dermatitis. In immunohistochemical analysis, CD80 and/or CD86 were detected on dendritic-shaped cells not only in the epidermis but also in the dermis in the inflammatory lesions of atopic dermatitis (n = 12). CD80 was expressed in only five cases (42%), while CD86 was expressed in all cases (100%). These molecules were not detected in normal control subjects (n = 8). In non-lesional skin of atopic dermatitis (n = 4), CD86 but not CD80 was detected in one case. CD86 was preferentially induced on dendritic-shaped cells in positive patch test sites to Dermatophagoides pteronyssinus or house dust allergen in atopic dermatitis (n = 4). The CD80- or CD86-positive cells were confirmed as Langerhans cells by double immunostaining using anti-CD1a monoclonal antibody. Neither CD86 nor CD80 was detected on keratinocytes. Similar results of the stronger expression of CD86 over that of CD80 were obtained from psoriasis vulgaris (n = 11) and from contact dermatitis (n = 7), although CD86 was expressed only in 57% of the contact dermatitis cases. The percentage of Langerhans cells positive for CD86 was higher than for CD80, i.e. 48% compared with 9%, respectively, in the epidermis of lesional skin of atopic dermatitis (n = 8). The expression rate of these molecules on Langerhans cells increased in the dermis. To investigate the function of co-stimulatory molecules on Langerhans cells in atopic dermatitis, we conducted an inhibition test with antibodies. Anti-CD86 monoclonal antibody almost completely inhibited T-cell proliferation stimulated with crude extract of D. pteronyssinus in the presence of epidermal cells as antigen-presenting cells, whereas anti-CD80 monoclonal antibody produced less of an inhibitory effect. These data indicate that CD86 expressed on Langerhans cells may play an important part in the pathogenesis of atopic dermatitis.
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