L3T4+ and Lyt-2+ cell-surface antigens as indicators of an allergic contact hypersensitivity response

Stern, M.; Muson, A. E.

doi:10.1007/bf00372623

Cited by 1 publication

(1 citation statement)

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“…T-cell infiltra tion started not before 24 h and was much less pronounced than macrophage infiltration. This is dis tinct from contact allergy in humans, where T-cell in filtration seems to predominate [21; and unpublished observation], A suppression of immune response dur ing the course of allergy may be indicated by increas ing numbers of Lyt-2-l-cells [22], At 24 and 48 h most of the T cells were CD4+, later CD8+ cells prevailed. Surprisingly, the percentage of ICAM-1 + infiltrating cells was not as high as expected from in vitro data.…”

Section: Discussionmentioning

confidence: 99%

Expression of Intercellular Adhesion Molecule-1 in Murine Allergic Contact Dermatitis

Goebeler¹,

Gutwald²,

Roth³

et al. 1990

Int Arch Allergy Immunol

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Intercellular adhesion molecule-1 (ICAM-1) plays an important role in the interaction of immunocompetent cells in inflammation. It contributes to lymphocyte recruitment, antigen presentation and T-cell activation. Recently, the murine homologue of ICAM-1, originally designated as MALA-2, has been identified. The monoclonal antibody YN1/1.7 for murine ICAM-1 enables the analysis of ICAM-1 expression in murine allergic contact dermatitis, a prototype of cutaneous T-cell-mediated inflammatory response. At 0, 1, 8, 24, 48, 72 h, and 7 and 14 days after challenge with 2,4-dinitrofluoro-1-benzene (DNFB) cryostat sections of ear skin were immunostained for ICAM-1, I-A and mononuclear cells (L3T4, Lyt-2, BM8). In normal skin ICAM-1 labeling was restricted to endothelial cells and dermal dendritic cells/macrophages; keratinocytes (KCs) did not express ICAM-1. The dermal cellular infiltrate increased progressively from 8 to 72 h after DNFB challenge. The majority of infiltrating cells were BM8+ macrophages (75%) and L3T4+ (10%) or Lyt-2 + T cells (10%); maximally 30% of those stained positive for ICAM-1. At 24 h, focal ICAM-1 expression on KCs developed, reached a maximum at 72 h and faded therafter. Migration of T cells into the epidermal layer started at 48 h at sites which had already expressed ICAM-1. Our data provide evidence that expression of ICAM-1 by epidermal cells precedes infiltration of the epidermis by T lymphocytes as shown before in human cutaneous disorders. Thus, a mouse model may be useful to investigate the role of ICAM-1 in inflammation further.

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Section: Discussionmentioning

confidence: 99%