Dermal mast cells determine susceptibility to ultraviolet B-induced systemic suppression of contact hypersensitivity responses in mice
Open accessAbstract
Different strains of mice have varying susceptibilities to ultraviolet radiation (UV) of wavelength 280–320 nm (UVB) for 50% suppression of systemic contact hypersensitivity (CHS) responses. Prevalence of histamine-staining dermal mast cells in different strains of mice (C57BL/ 6J, DBA/2, BALB/c) correlated directly with their susceptibility to UVB-induced systemic immunosuppression. BALB/c mice carrying Uvs1, a major locus for susceptibility to UV-induced immunosuppression, contained greater numbers of dermal mast cells than BALB/c mice of the same parental origin. Strains of mice that were differentiated on their susceptibility to UVB-induced downregulation of systemic CHS responses were similar in their susceptibility to histamine-induced immunomodulation. Histamine, but not UVB irradiation, decreased systemic CHS responses in mast cell–depleted mice (W f/W f). Reconstitution of the dorsal skin of W f/W f mice with bone marrow–derived mast cell precursors from nonmutant mice rendered the mice susceptible to UVB irradiation for systemic suppression of CHS responses. UVB irradiation did not suppress delayed type hypersensitivity responses to allogeneic spleen cells in W f/W f mice. In contrast, UV irradiation suppressed CHS responses in W f/W f mice when hapten was applied to the irradiated site. This study demonstrates that dermal mast cells are necessary for the induction of systemic suppression of CHS responses by UVB radiation, and suggests that mast cell– derived histamine is one component of this UVB-induced systemic immunosuppression.
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UV radiation and topical 1,25(OH)2D3 can activate dermal mast cells, which are important to determine the extent of UV immunomodulation.
“For example, UV radiation and topical 1,25(OH)2D3 can also activate dermal mast cells [88,89], which are important to determine the extent of UV immunomodulation [89,90].”
From Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy (2013) · cites this paper as [89]
The paper states that dermal mast cells are activated after UVB irradiation and reports in the Discussion (page not provided) that their prevalence correlates with susceptibility to UVB-induced systemic immunomodulation in mice. It does not address activation by topical 1,25(OH)2D3, and its finding about mast cells concerns systemic rather than local suppression. (LLM, conf=0.87)
Experimental — accuracy not yet measuredDermal mast cells are important determinants of the extent of UV immunomodulation.
“which are important determinants of the extent of UV immunomodulation [89,90].”
From Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy (2013) · cites this paper as [89]
The Discussion reports that dermal mast cell prevalence correlated with susceptibility to UVB-induced systemic immunosuppression in mice, and that restoring mast cells conferred susceptibility. But it also reports no evidence of mast cell involvement in local UVB modulation of contact hypersensitivity, so the unqualified claim about UV immunomodulation is broader than the finding. (LLM, conf=0.85)
Experimental — accuracy not yet measuredUVR radiation and topical 1,25(OH)2D3 can activate dermal mast cells.
“In mast cells, UVR radiation and topical 1,25(OH)2D3 can also activate dermal mast cells [88,89]”
From Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy (2013) · cites this paper as [89]
The paper states that dermal mast cells are activated and degranulate after UVB irradiation (opening section; page unavailable), supporting the UVR part of the claim. Its Discussion says whether UV triggers degranulation directly or indirectly is uncertain. No passage found addresses topical 1,25(OH)2D3 or its effect on dermal mast cells. (LLM, conf=0.88)
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Research works printed but not linked: 34
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- Authors
- Hart, P. H., Grimbaldeston, M. A., Swift, G. J., Jaksic, A., Noonan, F. P., & Finlay-Jones, J. J.
- Affiliations
- Flinders University (AU)
- From the *Department of Microbiology and Infectious Diseases, School of Medicine, Flinders University of South Australia, Adelaide, Australia 5001; and the ‡Department of Dermatology, The George Washington University, Washington, District of Columbia 20037
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 1998-06-15
- Volume
- 187
- Issue
- 12
- Pages
- 2045-2053
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2212357
- OpenAlex
- W2064990965
- Cited by
- 241
- References
- 0
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 5 · 2023: 6 · 2022: 3 · 2021: 6 · 2020: 4 · 2019: 7 · 2018: 4 · 2017: 10 · 2016: 15 · 2015: 12 · 2014: 12 · 2013: 9 · 2012: 8
- FWCI
- 3.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- Flinders Medical Centre Foundation
- National Institutes of Health
- National Cancer Institute (R01 CA-53765, R01CA053765)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- dermal mast cells, UV-B radiation, systemic immunosuppression, contact hypersensitivity, histamine, mast cell depletion, delayed-type hypersensitivity, hapten sensitization, BALB/c mice
- MeSH terms
- Animals, Bone Marrow Cells, Dermatitis, Contact, Female, Hypersensitivity, Delayed, Immunosuppression Therapy, Mast Cells, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Inbred DBA, Radiation Tolerance, Skin, Ultraviolet Rays, Microscopy, Video, Stem Cell Transplantation, Mice
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