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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15 June 1998
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June 15 1998
Dermal Mast Cells Determine Susceptibility to Ultraviolet B–induced Systemic Suppression of Contact Hypersensitivity Responses in Mice
Prue H. Hart,
Prue H. Hart
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
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Michele A. Grimbaldeston,
Michele A. Grimbaldeston
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
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Georgina J. Swift,
Georgina J. Swift
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
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Aleksandra Jaksic,
Aleksandra Jaksic
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
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Frances P. Noonan,
Frances P. Noonan
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
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John J. Finlay-Jones
John J. Finlay-Jones
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
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Prue H. Hart
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
Michele A. Grimbaldeston
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
Georgina J. Swift
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
Aleksandra Jaksic
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
Frances P. Noonan
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
John J. Finlay-Jones
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
Address correspondence to P.H. Hart, Department of Microbiology and Infectious Diseases, School of Medicine, Flinders University of South Australia, GPO Box 2100, Adelaide, Australia 5001. Phone: 61-8-82045404; Fax: 61-8-82768658; E-mail: [email protected]
Received:
February 04 1998
Online ISSN: 1540-9538
Print ISSN: 0022-1007
1998
J Exp Med (1998) 187 (12): 2045–2053.
Article history
Received:
February 04 1998
Citation
Prue H. Hart, Michele A. Grimbaldeston, Georgina J. Swift, Aleksandra Jaksic, Frances P. Noonan, John J. Finlay-Jones; Dermal Mast Cells Determine Susceptibility to Ultraviolet B–induced Systemic Suppression of Contact Hypersensitivity Responses in Mice . J Exp Med 15 June 1998; 187 (12): 2045–2053. doi: https://doi.org/10.1084/jem.187.12.2045
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