Keratinocyte intercellular adhesion molecule-1 (ICAM-1) expression precedes dermal T lymphocytic infiltration in allergic contact dermatitis (Rhus dermatitis) - PubMed (original) (raw)
. 1989 Dec;135(6):1045-53.
Affiliations
- PMID: 2574536
- PMCID: PMC1880503
Keratinocyte intercellular adhesion molecule-1 (ICAM-1) expression precedes dermal T lymphocytic infiltration in allergic contact dermatitis (Rhus dermatitis)
C E Griffiths et al. Am J Pathol. 1989 Dec.
Abstract
The ability of small molecules such as urushiol, present as a wax on the poison ivy leaf surface, to cause allergic contact dermatitis (rhus dermatitis) has fascinated immunologists for decades. Current dogma suggests that these epicutaneously applied catechol-containing molecules serve as haptens to conjugate with larger proteins via reactive o-quinone intermediates. These complexes are then recognized as foreign antigens by the immune system and elicit a hypersensitivity reaction. Phorbol ester can directly induce cultured keratinocyte (KC) intercellular adhesion molecule-1 (ICAM-1) expression via a protein kinase C (PK-C)-dependent mechanism. As urushiol is also a known PK-C agonist, we asked if topical application of a poison ivy/oak mixture could directly induce epidermal KC ICAM-1 expression. During the pre-erythematous phase of this reaction (4 to 20 hours), epidermal KCs expressed ICAM-1; this "initiation phase" preceded the appearance of activated memory T lymphocytes in the papillary dermis, and thus appeared to be nonlymphokine mediated. A near-contiguous cellular-adhesion molecular network was identified by ICAM-1 staining of basal KCs, dermal dendrocytes, and endothelial cells. During the second 24-hour period with the onset of erythema and edema, there was an "amplification phase" of more intense KC ICAM-1 expression coupled with relatively weak KC HLA-DR expression that coincided with dermal and epidermal T-cell infiltration. This suggests the presence of lymphokines, such as gamma interferon, during the amplification phase because of KC HLA-DR expression. On cultured KCs, urushiol directly induced ICAM-1 expression but not HLA-DR. Thus, in addition to functioning as an antigenic hapten, urushiol directly induces KC ICAM-1 expression. The KC ICAM-1 expression may then alter the dynamic trafficking of memory T cells in the epidermis, so as to initiate cutaneous inflammation in a nonantigen specific manner. This initiation phase is followed by T-cell infiltration and consequent lymphokine production that significantly amplifies the original stimulus. Thus much can still be learned about the molecular pathophysiology of this common type of cutaneous inflammation.
Similar articles
- Modulation of leucocyte adhesion molecules, a T-cell chemotaxin (IL-8) and a regulatory cytokine (TNF-alpha) in allergic contact dermatitis (rhus dermatitis).
Griffiths CE, Barker JN, Kunkel S, Nickoloff BJ. Griffiths CE, et al. Br J Dermatol. 1991 Jun;124(6):519-26. doi: 10.1111/j.1365-2133.1991.tb04943.x. Br J Dermatol. 1991. PMID: 1712219 - Differential modulation of keratinocyte intercellular adhesion molecule-I expression by gamma interferon and phorbol ester: evidence for involvement of protein kinase C signal transduction.
Griffiths CE, Esmann J, Fisher GJ, Voorhees JJ, Nickoloff BJ. Griffiths CE, et al. Br J Dermatol. 1990 Mar;122(3):333-42. doi: 10.1111/j.1365-2133.1990.tb08281.x. Br J Dermatol. 1990. PMID: 1969746 - Histamine and cis-urocanic acid augment tumor necrosis factor-alpha mediated induction of keratinocyte intercellular adhesion molecule-1 expression.
Mitra RS, Shimizu Y, Nickoloff BJ. Mitra RS, et al. J Cell Physiol. 1993 Aug;156(2):348-57. doi: 10.1002/jcp.1041560218. J Cell Physiol. 1993. PMID: 8102141 - Vesicular Contact Reaction May Progress into Erythema Multiforme.
Czarnecka-Operacz M, Jenerowicz D, Szulczyńska-Gabor J, Teresiak-Mikołajczak E, Szyfter-Harris J, Bowszyc-Dmochowska M. Czarnecka-Operacz M, et al. Acta Dermatovenerol Croat. 2016 Dec;24(4):307-309. Acta Dermatovenerol Croat. 2016. PMID: 28128086 Review. - The role of adhesion molecules, chemotactic factors, and cytokines in inflammatory and neoplastic skin disease--1990 update.
Nickoloff BJ, Griffiths CE, Barker JN. Nickoloff BJ, et al. J Invest Dermatol. 1990 Jun;94(6 Suppl):151S-157S. doi: 10.1111/1523-1747.ep12876134. J Invest Dermatol. 1990. PMID: 2191050 Review.
Cited by
- Silver Nanoparticles Biocomposite Films with Antimicrobial Activity: In Vitro and In Vivo Tests.
Cadinoiu AN, Rata DM, Daraba OM, Ichim DL, Popescu I, Solcan C, Solcan G. Cadinoiu AN, et al. Int J Mol Sci. 2022 Sep 14;23(18):10671. doi: 10.3390/ijms231810671. Int J Mol Sci. 2022. PMID: 36142584 Free PMC article. - Unraveling the Role of Sex Hormones on Keratinocyte Functions in Human Inflammatory Skin Diseases.
Gratton R, Del Vecchio C, Zupin L, Crovella S. Gratton R, et al. Int J Mol Sci. 2022 Mar 15;23(6):3132. doi: 10.3390/ijms23063132. Int J Mol Sci. 2022. PMID: 35328552 Free PMC article. Review. - Skin Immunity and Tolerance: Focus on Epidermal Keratinocytes Expressing HLA-G.
Mestrallet G, Rouas-Freiss N, LeMaoult J, Fortunel NO, Martin MT. Mestrallet G, et al. Front Immunol. 2021 Dec 6;12:772516. doi: 10.3389/fimmu.2021.772516. eCollection 2021. Front Immunol. 2021. PMID: 34938293 Free PMC article. Review. - Allergens of the urushiol family promote mitochondrial dysfunction by inhibiting the electron transport at the level of cytochromes b and chemically modify cytochrome c1.
Pacheco R, Quezada SA, Kalergis AM, Becker MI, Ferreira J, De Ioannes AE. Pacheco R, et al. Biol Res. 2021 Oct 28;54(1):35. doi: 10.1186/s40659-021-00357-z. Biol Res. 2021. PMID: 34711292 Free PMC article. - Extracellular Vesicles Released From the Skin Commensal Yeast Malassezia sympodialis Activate Human Primary Keratinocytes.
Vallhov H, Johansson C, Veerman RE, Scheynius A. Vallhov H, et al. Front Cell Infect Microbiol. 2020 Jan 24;10:6. doi: 10.3389/fcimb.2020.00006. eCollection 2020. Front Cell Infect Microbiol. 2020. PMID: 32039038 Free PMC article.
References
- Science. 1982 Mar 5;215(4537):1239-41 - PubMed
- Adv Dermatol. 1988;3:293-307 - PubMed
- Biochemistry. 1985 Feb 12;24(4):999-1007 - PubMed
- Proc Natl Acad Sci U S A. 1986 May;83(9):2914-8 - PubMed
- Eur J Immunol. 1988 Sep;18(9):1397-404 - PubMed
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Research Materials
Miscellaneous