Contact allergens and epidermal proinflammatory cytokines modulate Langerhans cell E-cadherin expression in situ

Research output: Contribution to journalArticle

149 Citations (Scopus)

Abstract

After exposure to antigen, Langerhans cells (LC) migrate from the epidermis to lymph nodes, where they initiate primary immune responses in T cells. The adhesion molecule E-cadherin mediates adhesion of LC to keratinocytes in vitro and may be responsible for localization of LC in epidermis. To determine? if levels of LC E-cadherin are modulated during LC emigration from epidermis, we utilized how cytometry to evaluate E-cadherin expression on BALB/c LC exposed in situ to the contact allergen 2,4,6-trinitrochlorobenzene (TNCB). TNCB induced increased I-A/E antigen and decreased E-cadherin expression on a subpopulation of LC as early as 12 h, and as late as 48 h, after application. At 24 h, ~ 30% of LC in TNCB-treated skin expressed increased I-A/E antigens; of these activated LC, ~ 40% expressed decreased levels of E-cadherin. E-cadherin levels on this latter subset were ~ 15% of those expressed by LC in normal skin, and were similar to levels on cultured LC and LC that migrated from skin explants. The effect was specific for allergens; no changes occurred in LC following treatment with several contact irritants or the tolerogen dinitrathiocyanobenzene. To determine if cytokines modulated LC E-cadherin expression, we introduced various cytokines into BALB/c ear skin and assayed I-A/E antigen and E-cadherin levels. Of the cytokines tested, only interleukin-1 and tumor necrosis factor a reproduced the effects of TNCB. We propose that downmodulation of E-cadherin expression occurs as a consequence of local cytokine production during antigen-induced LC activation, facilitating LC emigration and the initiation of immune responses against antigens encountered in epidermis.

Original languageEnglish (US)
Pages (from-to)553-558
Number of pages6
JournalJournal of Investigative Dermatology
Volume106
Issue number3
DOIs
StatePublished - Jan 1 1996
Externally publishedYes

Fingerprint

Langerhans Cells
Cadherins
Allergens
Cytokines
Picryl Chloride
Antigens
Skin
Histocompatibility Antigens Class II
Epidermis
Adhesion
Emigration and Immigration
T-cells
Irritants
Interleukin-1
Tumor Necrosis Factor-alpha
Chemical activation
Molecules
Keratinocytes

Keywords

  • Activation
  • Adhesion
  • Leukocyte
  • Migration

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology
  • Cell Biology

Cite this

Contact allergens and epidermal proinflammatory cytokines modulate Langerhans cell E-cadherin expression in situ. / Schwarzenberger, Kathryn; Udey, Mark C.

In: Journal of Investigative Dermatology, Vol. 106, No. 3, 01.01.1996, p. 553-558.

Research output: Contribution to journalArticle

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abstract = "After exposure to antigen, Langerhans cells (LC) migrate from the epidermis to lymph nodes, where they initiate primary immune responses in T cells. The adhesion molecule E-cadherin mediates adhesion of LC to keratinocytes in vitro and may be responsible for localization of LC in epidermis. To determine? if levels of LC E-cadherin are modulated during LC emigration from epidermis, we utilized how cytometry to evaluate E-cadherin expression on BALB/c LC exposed in situ to the contact allergen 2,4,6-trinitrochlorobenzene (TNCB). TNCB induced increased I-A/E antigen and decreased E-cadherin expression on a subpopulation of LC as early as 12 h, and as late as 48 h, after application. At 24 h, ~ 30{\%} of LC in TNCB-treated skin expressed increased I-A/E antigens; of these activated LC, ~ 40{\%} expressed decreased levels of E-cadherin. E-cadherin levels on this latter subset were ~ 15{\%} of those expressed by LC in normal skin, and were similar to levels on cultured LC and LC that migrated from skin explants. The effect was specific for allergens; no changes occurred in LC following treatment with several contact irritants or the tolerogen dinitrathiocyanobenzene. To determine if cytokines modulated LC E-cadherin expression, we introduced various cytokines into BALB/c ear skin and assayed I-A/E antigen and E-cadherin levels. Of the cytokines tested, only interleukin-1 and tumor necrosis factor a reproduced the effects of TNCB. We propose that downmodulation of E-cadherin expression occurs as a consequence of local cytokine production during antigen-induced LC activation, facilitating LC emigration and the initiation of immune responses against antigens encountered in epidermis.",
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