Modulation of leucocyte adhesion molecules, a T-cell chemotaxin (IL-8) and a regulatory cytokine (TNF-Α) in allergic contact dermatitis (rhus dermatitis)
dc.contributor.author | Griffiths, Christopher E. M. | en_US |
dc.contributor.author | Barker, Jonathan N.W.N. | en_US |
dc.contributor.author | Kunkel, S. | en_US |
dc.contributor.author | Nickoloff, Brian J. | en_US |
dc.date.accessioned | 2010-06-01T18:14:54Z | |
dc.date.available | 2010-06-01T18:14:54Z | |
dc.date.issued | 1991-06 | en_US |
dc.identifier.citation | GRIFFITHS, C.E.M.; BARKER, J.N.W.N.; KUNKEL, S.; NICKOLOFF, B.J. (1991). "Modulation of leucocyte adhesion molecules, a T-cell chemotaxin (IL-8) and a regulatory cytokine (TNF-Α) in allergic contact dermatitis (rhus dermatitis)." British Journal of Dermatology 124(6): 519-526. <http://hdl.handle.net/2027.42/71459> | en_US |
dc.identifier.issn | 0007-0963 | en_US |
dc.identifier.issn | 1365-2133 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/71459 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=1712219&dopt=citation | en_US |
dc.description.abstract | To understand the molecular events which are important in leucocyte trafficking in cutaneous inflammation, poison ivy/oak extract was applied topically to the skin, and the simultaneous assessment of a variety of clinical and immunopathological parameters performed. The clinical response of subjects was divided into three main groups: I. 2–24 h after application, before the onset of erythema; II, 48 h-1 week after application during maximal clinical changes; III, 2–3 weeks after application when the inflammation had subsided. Six different biopsies per subject were evaluated over the study period and the density of dermal cellular infiltrate, and the distribution of intercellular adhesion molecule-1, (ICAM-1), endothelial leucocyte adhesion molecule-1, (ELAM-1), vascular cell adhesion molecule-1, (VCAM-1), interleukin 8 (IL-8) and tumour necrosis factor-alpha (TNF-Α), determined. Eight hours after exposure, before lymphocytes and monocytes had entered the dermal interstitium or epidermis, the keratinocytes expressed TNF-Α and TCAM-1, whilst the endothelial cells expressed ELAM-1, VCAM-1 and ICAM-1. Group II biopsies revealed increasing keratinocyte expression of TNF-Α and ICAM-1 with the appearance of IL-8, which correlated with the onset of epidermal T-cell trafficking. The endothelium was strongly positive for ELAM-1 and VCAM-1, but there was no influx of neutrophils. Group III biopsies showed a decrease in the expression of ICAM-1, VCAM-1 and FLAM-1 by both keratinocytes and endothelium with a reduction in epidermal/dermal inflammation, although the endothelial cell staining of VCAM-1 and ELAM-1 did not completely disappear. These results suggest that on exposure to poison ivy/oak, keratinocytes rapidly produce TNF-Α which leads to an early autoinduction of ICAM-1, and later IL-8. There is also a paracrine-mediated induction and augmentation of underlying endothelial cell ELAM-1, VCAM-1 and ICAM-1. | en_US |
dc.format.extent | 2331153 bytes | |
dc.format.extent | 3109 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Blackwell Publishing Ltd | en_US |
dc.rights | 1991 British Association of Dermatologists | en_US |
dc.title | Modulation of leucocyte adhesion molecules, a T-cell chemotaxin (IL-8) and a regulatory cytokine (TNF-Α) in allergic contact dermatitis (rhus dermatitis) | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Dermatology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | * Department of Dermatology, University of Michigan, 1301 Catherine Road, Medical Science I Building Box 0602, Arm Arbor, Michigan 48109-0602, U.S.A. | en_US |
dc.contributor.affiliationum | † Department of Pathology, University of Michigan, 1301 Catherine Road, Medical Science I Building Box 0602, Arm Arbor, Michigan 48109-0602, U.S.A. | en_US |
dc.identifier.pmid | 1712219 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/71459/1/j.1365-2133.1991.tb04943.x.pdf | |
dc.identifier.doi | 10.1111/j.1365-2133.1991.tb04943.x | en_US |
dc.identifier.source | British Journal of Dermatology | en_US |
dc.identifier.citedreference | Dvorak AM, Mihim MC Jr, Dvorak HF. Morphology of delayed type hypersensitivity reactions in man. II. Ultrastructural alterations affecting the microvasculature. Lab Invest 1976; 34: 179 – 91. | en_US |
dc.identifier.citedreference | Griffiths CEM, Nickoloff BJ. Keratinocyte intercellular adhesion molecule-1 (ICAM-1) expression precedes dermal T lymphocytic infiltration in allergic contact dermatitis (Rhus dermatitis). Am J Pathol 1989; 135: 1045 – 53. | en_US |
dc.identifier.citedreference | Barker JNWN, Sarma V, Mitra RS et al. Marked synergism between TNF-Α and IFN-Γ in regulation of keratinocyte-derived adhesion molecules and chemotactic factors. J Clin Invest 1990; 85: 605 – 8. | en_US |
dc.identifier.citedreference | Barker JNWN, Griffiths CEM, Dixit VM, Nickoloff BJ. Keratinocytes as initiators of inilammation. Lancet 1991; 337: 211 – 14. | en_US |
dc.identifier.citedreference | Carlos TM, Schwartz BR, Kovach NL et al. Vascular cell adhesion molecule-1 (VCAM-1) mediates lymphocyte adherence to cytokine-activated cultured human endothelial cells. Blood 1990; 76: 965 – 70. | en_US |
dc.identifier.citedreference | Cotran RS, Gimbrone MA, Bevilacqua MP et al. Induction and detection of a human endothelial activation antigen in vivo. J Exp Med 1986; 164: 661 – 6. | en_US |
dc.identifier.citedreference | Rice GE, Munro JM, Bevilacqua MP. Inducible cell adhesion molecule 110 (INCAM-110) is an endothelial receptor for lymphocytes. J Exp Med 1990; 171: 1369 – 74. | en_US |
dc.identifier.citedreference | Nickoloff BJ, Karabin GD, Barker JNWN et al. Molecular and cellular localization of IL-8 and its inducer—TNF-Α in psoriasis. Am J Pathol 1991; 138: 129 – 40. | en_US |
dc.identifier.citedreference | Cerio R, Griffiths CEM, Cooper KD et al. Characterization of factor XIIIa positive dermal dendritic cells in normal and inflamed skin. Br J Dermatol 1989; 121: 421 – 31. | en_US |
dc.identifier.citedreference | Sontheimer RD. Perivascular dendritic macrophages as immuno-biological constituents of the human dermal microvascular unit. J Invest Dermatol 1989; 93 ( Suppl. ): 96 – 101. | en_US |
dc.identifier.citedreference | Pober JS. Cytokine mediated activation of vascular endothelium: Physiology and pathology. Am J Pathol 1988; 131: 426 – 33. | en_US |
dc.identifier.citedreference | Griffiths CEM, Voorhees JJ, Nickoloff BJ. Characterization of intercellular adhesion molecule-1 and HLA-DR in normal and inflamed skin: Modulation by recombinant interferon-gamma and tumor necrosis factor. J Am Acad Dermatol 1989; 20: 617 – 29. | en_US |
dc.identifier.citedreference | Pober JS, Bevilacqu MP, Mendrick DL et al. Two distinct monokines, interleukin-1 and tumor necrosis factor, each independently induce biosynthesis and transient expression of the same antigen on the surface of cultured human vascular endothelial cells. J Immunol 1986; 136: 1680 – 7. | en_US |
dc.identifier.citedreference | Osborn L, Hession C, Tizzard R et al. Direct expression cloning of vascular Cell adhesion molecule 1, a cytokine-induced endothelial protein that binds to lymphocytes. Cell 1989; 59: 1203 – 11. | en_US |
dc.identifier.citedreference | Dustin ML, Springer TA. Lymphocyte function associated antigen-1 (LFA-1) interaction with intercellular adhesion molecule-1 (ICAM-1) is one of at least three mechanisms for lymphocyte adhesion to cultured endothelial cells. J Cell Biol 1988; 107: 321 – 31. | en_US |
dc.identifier.citedreference | Stoolman LM. Adhesion molecules controlling lymphocyte migration. Cell 1989; 56: 907 – 10. | en_US |
dc.identifier.citedreference | Nickoloff BJ, Griffiths CEM, Barker JNWN. The role of adhesion molecules, chemotactic factors, and cytokines in inflammatory and neoplastic skin disease—1900 update. J Invest Dermatol 1990; 94 ( Suppl. ): 151 – 7. | en_US |
dc.identifier.citedreference | Bevilacqua MP, Pober JS, Mendrick DL et al. Identification of an inducible endothelial-leukocyte adhesion molecule. Proc Natl Acad Sci USA 1987; 84: 9238 – 42. | en_US |
dc.identifier.citedreference | Munro JM, Pober JS, Cotran RS. Tumor necrosis factor and interferon-Γ induce distinct patterns of endothelial activation and associated leukocyte accumulation in skin of Papio anubis. Am J Pathol 1989; 135: 121 – 33. | en_US |
dc.identifier.citedreference | Messadi DV, Pober JS, Fiers W et al. Induction of an activation antigen on post capillary venular endothelium in human skin organ culture. J Immunol 1987; 139: 1557 – 62. | en_US |
dc.identifier.citedreference | Ho VC, Griffiths CEM, Ellis CN et al. Intralesional cyclosporine A in the treatment of psoriasis: A clinical, immunologic and pharmacokinetic study. J Am Acad Dermatol 1990; 22: 94 – 100. | en_US |
dc.identifier.citedreference | Ho VC, Gupta AK, Ellis CN et al. Treatment of severe lichen planus with cyclosporin A. J Am Acad Dermatol 1990; 22: 64 – 8. | en_US |
dc.identifier.citedreference | Gupta AK, Ellis CN, Cooper KD el al. Oral cyclosporine A for the treatment of alopecia areata. J Am Acad Dermatol 1990; 22: 242 – 50. | en_US |
dc.identifier.citedreference | Nickoloff BJ. The role of gamma interferon in cutaneous trafficking of lymphocytes with emphasis on molecular and cellular adhesion events. Arch Dermatol 1988; 124: 1835 – 43. | en_US |
dc.identifier.citedreference | Willms-Kretschmer K, Flax MH, Cotran RS. The fine structure of the vascular response in hapten-specific delayed hypersensitivity and contact dermatitis. Lab Invest 1967; 17: 334 – 9. | en_US |
dc.identifier.citedreference | Larsen CG, Anderson AO, Oppenheim JJ, Matsushima K. Production of interleukin-8 by human dermal fibroblasts and keratinocytes in response to interleukin-1 or tumor necrosis factor. Immunology 1989; 68: 31 – 6. | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
Files in this item
Remediation of Harmful Language
The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.
Accessibility
If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.