Open AccessFunctional characterization of skin‐infiltrating lymphocytes in atopic dermatitis
Author(s) -
REINHOLD U.,
KUKEL S.,
GOEDEN B.,
NEUMANN U.,
KREYSEL H. W.
Publication year - 1991
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1991.tb02951.x
Subject(s) - ionomycin , immunology , immune system , tumor necrosis factor alpha , cytotoxic t cell , cytokine , secretion , t cell , interleukin 4 , biology , stimulation , in vitro , microbiology and biotechnology , medicine , endocrinology , biochemistry
SUMMARY Skin‐infiltrating lymphocytes (SIL) were isolated from skin biopsies of patients with hyperimmunoglobulin E (IgE) atopic dermatitis (AD) and expanded in vitro in the presence of IL‐2 in combination with IL‐4. Phenotypic analysis of skin‐derived cells revealed the predominance of CD4 + T helper/inducer phenotype in SIL populations. In 3 H‐thymidine incorporation assays, SIL showed proliferation in response to IL‐2, IL‐3, IL‐4, ionomycin (Io)+ 12‐ o ‐tetradecanoyl‐phorbol‐13‐acetate (TPA) and OKT3 + TPA. OKT4 with and without TPA did not induce proliferation. Tumour necrosis factor alpha (TNF‐α) did not block proliferative responses of SIL to IL‐2 and IL‐4. Cultured SIL showed no cytotoxic activity against K562 and Jurkat target cells. Expanded skin‐derived T cells were tested for their capacity to secrete several cytokines in vitro . SIL secreted significant amounts of IL‐4, GM‐CSF and TNF‐α upon stimulation with mitogens but failed to secrete IFN‐γ. Io in combination with phorbolester induced the secretion of larger amounts of IL‐4, GM‐CSF, TNF‐α and low amounts of IFN‐γ. The data indicate that SIL derived from AD lesions were defective in their capacity to secrete IFN‐γ but were enriched in T cells capable of producing IL‐4 upon stimulation. The results support the possibility of a predominant‘T H2 ‐like’ cell‐mediated immune response in lesional skin of AD patients.