Skin cancer. Introduction.
Explore the source record for details and available documents.
Carcinoma, Squamous Cell↗
Biomedical subjects
M L Kripke
Publications and source records attributed to M L Kripke.
DNA repair capacity correlates with mutagen sensitivity in lymphoblastoid cell lines.
This study describes a correlation between cellular DNA repair capacity and the frequency of mutagen-induced in vitro chromosomal breaks in selected lymphoblastoid cell lines. Two assays, host cell reactivation (HCR) assay for measuring cellular DNA repair capacity and in vitro mutagen sensitivity assay, have recently been shown to be useful biomarkers for such susceptibility. Increased in vitro mutagen sensitivity, measured by the number of induced chromatid breaks, has been postulated to reflect decreased capacity of DNA repair, as measured by the HCR assay. However, these two assays have not been examined in parallel to test this hypothesis. In this study, we performed both assays in 16 established lymphoblastoid cell lines derived from patients with xeroderma pigmentosum (n = 3), ataxia telangiectasia (n = 2), head and neck cancer (n = 3), and melanoma (n = 2), and from normal human subjects (n = 6) using UV light, 4-nitroquinoline-1-oxide (4-NQO; an UV-mimetic agent), and gamma-irradiation as the test agents. The measurements from the HCR assay correlated significantly with the frequency of chromatid breaks induced by either UV irradiation (r = -0.69; P < 0.01) or 4-NQO (r = -0.70; P < 0.01). Although published data suggest that damage induced by UV and 4-NQO may be repaired by different pathways, the two agents induced similar frequencies of chromatid breaks (r = 0.68; P < 0.01) in the tested cell lines. Our results also indicated that the HCR assay is not suitable to test agents that cause DNA strand breaks, such as gamma-irradiation, whereas the mutagen sensitivity assay is. Although reduced cellular DNA repair capacity correlated with increased frequency of mutagen-induced chromatid breaks in these cell lines, these two assays have different sensitivities in measuring the repair of damage induced by different carcinogens; therefore, the use of both assays is recommended for future molecular epidemiological studies of cancer susceptibility.
4-Nitroquinoline-1-oxide↗
The immune system in ultraviolet carcinogenesis.
The immune system plays an important role in ultraviolet (UV) carcinogenesis by contributing to host resistance against skin cancer development. UV radiation, however, circumvents immune surveillance against skin cancers by modulating the immune response in a way that favors tumor development. Studies addressing the cellular mechanisms by which UV radiation modifies immune function are summarized. These studies demonstrate that UV irradiation of the skin produces both local, nonspecific immune suppression that inhibits immune effector functions within irradiated skin, as well as systemic, specific immune suppression against antigens introduced at a critical time after exposure to UV radiation. Evidence is presented suggesting that the production of cytokines by epidermal cells in response to UV-induced DNA damage is an important component of UV-induced specific immune suppression.
Animals↗
p53 mutations in nonmelanoma skin cancer of the head and neck: molecular evidence for field cancerization.
Multiple and distinct p53 mutations were detected by DNA sequence analysis in tumor and adjacent nonmalignant skin samples from eight patients with nonmelanoma skin cancer of the head and neck, providing unambiguous evidence for field cancerization. The mutations consisted of C-->T transitions at dipyrimidine sequences (30% of all single base substitutions), T-->C transitions (47%), and G-->T transversions (12%), suggesting that other carcinogens may act along with UV radiation in the development of nonmelanoma skin cancer. Patient interviews revealed that, in addition to substantial exposure to solar UV radiation, most had a history of smoking and were exposed to carcinogens from industrial or agricultural sources. These data show that extensive molecular epidemiological investigations are necessary to elucidate risk factors associated with the disease in localities where patients often report substantial exposure to environmental carcinogens.
Adult↗
Modulation of immunity to Borrelia burgdorferi by ultraviolet irradiation: differential effect on Th1 and Th2 immune responses.
Ultraviolet B (UVB) radiation suppresses the delayed-type hypersensitivity (DTH) response to alloantigen by a mechanism involving interleukin (IL)-10. It has been hypothesized, based on this result, that UV irradiation shifts the immune response from a Th1 to a Th2 response. We tested this hypothesis using Borrelia burgdorferi (Bb) as an antigen under conditions where both DTH and antibody responses could be assessed. Mice were irradiated with a single dose of UV and then immunized with Bb in complete Freund's adjuvant (CFA). DTH was assessed by footpad challenge. At various time points thereafter, mice were bled, and the serum antibodies to Bb were quantitated. Only IgG1, IgG2a, and IgG2b were produced in response to Bb. The IgG2a and IgG2b antibody responses, as well as the DTH response to Bb, showed UV dose-dependent reductions after UV irradiation. The primary IgG1 response to Bb was very low and was unaffected by UV irradiation; however, the IgG1 secondary response was elevated in UV-irradiated mice. Injection of anti-IL-10 antibody into UV-irradiated mice within 24 h after UV exposure restored the DTH response, as well as the IgG2a and IgG2b antibody responses. In addition, injecting recombinant murine IL-10 mimicked some of the effects of UV radiation. Our results support the hypothesis that in vivo, UV irradiation down-regulates Th1 immune responses, while leaving Th2 responses intact, and suggest that IL-10 is an important mediator of this effect.
Animals↗
Ultraviolet radiation reduces phagocytosis and intracellular killing of mycobacteria and inhibits nitric oxide production by macrophages in mice.
Exposure of mice to a single or multiple low doses of ultraviolet radiation (UVR) decreases the induction of the delayed-type hypersensitivity (DTH) response to Mycobacterium bovis BCG and Mycobacterium lepraemurium (MLM) and impairs the clearance of bacteria from the lymphoid organs. This study is an attempt to address the mechanism by which UV radiation impairs the clearance of bacteria from the lymphoid organs by determining whether alterations in macrophage function such as ingestion and intracellular killing of mycobacteria or production of reactive nitrogen intermediates might be responsible for these effects. BALB/c or C3H/HeN mice were exposed to a single dose of UVB (280-320 nm) radiation ranging from 0.35 to 45 kJ/m2, and at regular intervals after irradiation, the peritoneal and splenic macrophages were collected, cultured, and infected with live BCG or MLM. Phagocytosis was assessed at 6 h by counting the number of acid-fast bacteria per macrophage after Ziehl-Neelsen staining. The rate of intracellular killing was assessed by lysing the macrophages at 6, 12, 24, and 48 h after BCG infection, plating the suspension on 7H11 agar, and counting the number of colony-forming units 21 days later. Similarly, the nitric oxide production, as measured by nitrite, by macrophages obtained from UVB-irradiated and nonirradiated mice in response to BCG was assessed. There was a significant reduction in the uptake of organisms by both peritoneal and splenic macrophages collected from UV-irradiated mice. The intracellular killing of organisms was also significantly reduced, as was the production of nitric oxide by peritoneal macrophages infected with BCG in vitro. These results indicate that UVR affects macrophage functions and are consistent with our hypothesis that impaired clearance of bacteria in vivo results from an alteration in macrophage function.
Animals↗
Deficient antigen presentation and Ts induction are separate effects of ultraviolet irradiation.
Ultraviolet-B irradiation of murine skin before contact sensitization alters the antigen-presenting activity of cells in the skin and draining lymph nodes (DLN), decreases the contact hypersensitivity (CHS) response, and induces hapten-specific Ts cells. We determined whether hapten-bearing antigen-presenting cells (APC) from the DLN of UV-irradiated mice induce Ts cells. APC from UV-irradiated, FITC-sensitized mice were isolated, and FITC+ cells were FACS-purified and injected into the hind footpads of naive, syngeneic mice. Unseparated and FACS-purified bright FITC+ cells (FITChi) from UV-irradiated mice induced Ts. However, dull (FITClo) FITC+ cells, T-cell-depleted FITChi cells, or DLN cells from C3H SCID mice failed to induce Ts. Injection of FITC-bearing DLN cells from nonirradiated mice into UV-irradiated recipients failed to immunize and induced Ts instead. Treatment of the UV-irradiated recipients with anti-TNF-alpha blocked these effects. Thus, transferable suppression is due to Thy-1+ cells, does not require UV-altered APC for induction, and may depend on TNF-alpha.
Animals↗
Ultraviolet radiation decreases the granulomatous response to lepromin in humans.
Ultraviolet radiation (UVR) modulates cellular immunity in humans and experimental animals and can interfere with immune responses against infectious agents in animal models. We used the lepromin reaction, a cell-mediated immune response to antigens of Mycobacterium leprae, to determine whether UVR affects the cellular immune response to an infectious agent in humans. We selected 29 healthy, lepromin-positive contacts of leprosy patients and determined their minimal erythema dose (MED) of UVR. Immediately afterward, each subject was injected with 0.1 ml of lepromin in two areas of the buttocks: one at the site that had received twice the MED of UVR and the other on the contralateral, unirradiated site. The irradiated site was given twice the MED every 4 d for a total of five treatments. One week after the last irradiation, both lepromin reactions were measured and biopsied. The size of the lepromin-induced granulomas was significantly reduced in the irradiated site, as was the number of lymphocytes. Immunohistochemical analysis showed a depletion in the number of infiltrating cells and a lower percentage of T cells, particularly the CD4+ subpopulation, in granulomas formed in UV-irradiated skin. This study demonstrates that local UV irradiation reduces the granulomatous reaction to lepromin in sensitized individuals. These findings are of clinical relevance because of the fundamental role played by the delayed-type hypersensitivity response in defense against intracellular pathogens and because of potential increases in the amount of UVR in sunlight reaching the earth's surface.
Adolescent↗
Cells with UV-specific DNA damage are present in murine lymph nodes after in vivo UV irradiation.
Ultraviolet radiation is absorbed in the skin, especially in the epidermis. After ultraviolet irradiation the number of major histocompatibility complex class II+, adenosine triphosphatase+ Langerhans cells and Thy-1+ dendritic epidermal cells in the epidermis decreases. Whether this decrease is due to migration of these cells or to loss of membrane markers is not clear. To address this question we have used the monoclonal antibody H3 directed against cyclobutyl thymine dimers-a form of DNA damage that is specifically induced by ultraviolet radiation-to investigate whether H3+ cells are present in the draining lymph nodes of the skin after ultraviolet irradiation of hairless, inbred mice (HRA/Skh). After a single dose of ultraviolet radiation (Westinghouse FS40, 1.5 kJ/m2), H3+ cells were present in the paracortex of the draining lymph nodes. No positive cells were found in the blood of irradiated mice. These results suggest that the H3+ cells in the lymph nodes originate from the skin. The number of H3+ cells in the draining lymph nodes increased the first 24 h after irradiation and then stabilized. Immunohistochemical double staining revealed that all H3+ cells were major histocompatibility complex II+, and that only a fraction of the cells were NLDC-145 positive. No V gamma 3 T-cell receptor bearing cells could be found in the lymph nodes after UV irradiation of the skin.
Animals↗
Sunscreens and T4N5 liposomes differ in their ability to protect against ultraviolet-induced sunburn cell formation, alterations of dendritic epidermal cells, and local suppression of contact hypersensitivity.
Exposure of skin to ultraviolet (UV) radiation can lead to diverse biologic effects, including inflammation, sunburn cell formation, alterations of cutaneous immune cells, and impaired induction of contact hypersensitivity responses. The molecular mechanisms of these UV-induced effects are not completely understood. We investigated the ability of sunscreens and liposomes containing the DNA excision repair enzyme T4 endonuclease V to prevent these effects of UV radiation. The use of T4N5 liposomes, which increase the repair of cyclobutyl pyrimidine dimers, provides an approach for assessing the role of DNA damage in the effects of UV radiation on the skin. Exposing C3H mice to 500 mJ/cm2 UVB radiation from FS40 sunlamps resulted in skin edema, sunburn cell formation, and morphologic alterations and decreased numbers of Langerhans cells and Thy-1+ dendritic epidermal T cells. In addition, the induction of contact hypersensitivity after application of 2,4-dinitrofluorobenzene on UV-irradiated skin was diminished by 80%. Applying sunscreens containing octyl-N-dimethyl-p-aminobenzoate, 2-ethylhexyl-p-methoxycinnamate, or benzophenone-3 before this dose of UV irradiation gave nearly complete protection against all of these effects of UV irradiation. In contrast, topical application of T4N5 liposomes after UV irradiation had no effect on UV-induced skin edema and only partially protected against sunburn cell formation and local suppression of contact hypersensitivity, although its ability to protect against alterations in dendritic immune cells was comparable to that of the sunscreens. These results suggest that DNA damage is involved in only some of the local effects of UV radiation on the skin. In addition, T4N5 liposomes may be a useful adjunct to sunscreens because they can reduce some of the deleterious effects of UV radiation on skin even after a sunburn has been initiated.
Animals↗
Ultraviolet radiation and immunology: something new under the sun--presidential address.
The carcinogenic activity of solar radiation has been known for nearly a century. However, within the past few years, we have realized that exposing the skin to sunlight also has profound immunological effects on the host and that these immunological changes can contribute to the development of skin cancer and alter host resistance to infectious diseases. These findings have led to the development of a new field of research, termed photoimmunology, which is concerned with the effects of UV radiation on immunological processes. Our interest in this field arose from studies on the antigenic properties of skin cancers induced in mice by chronic exposure to UV-B (280-320 nm) radiation. These cancers are highly antigenic and many are immunologically rejected upon transplantation to normal syngeneic recipients. In studying how these cancers were able to survive and grow in the primary host, we discovered that exposing the skin to UV radiation altered some types of immune responses, including the immune response against skin cancers. Studies on the nature and mechanism of the immunological alterations brought about by exposure to UV radiation suggested that UV-induced DNA damage triggers a cascade of events, leading ultimately to a state of antigen-specific, systemic T lymphocyte-mediated immunosuppression. Key components of this cascade are epidermal cytokines, which modulate the immune response to antigens introduced into the UV-irradiated host and divert the response toward a state of specific immunosuppression. The finding that UV radiation can redirect the immune response from an effector to a suppressor pathway has raised the possibility that immune responses to infectious diseases might also be influenced by exposure of the host to UV radiation. Interest in the health consequences of stratospheric ozone depletion, with its attendant increase in solar UV-B radiation, has stimulated recent investigations on the effects of UV radiation on the pathogenesis of infections in animal models and on immune responses in humans. In addition, attempts are being made to use information about UV-induced specific immunosuppression to eliminate unwanted immune responses, such as transplant rejection and graft-versus-host reactions. Thus, studies on the immunological effects of UV radiation are providing new information on how immune responses are regulated as well as improving our understanding of the role of the immune system in skin cancer induction. This information should facilitate the development of more effective measures for preventing the deleterious effects of overexposure to UV radiation.
Animals↗
Dendritic epidermal T cells inhibit T cell proliferation and may induce tolerance by cytotoxicity.
Hapten-conjugated cells of the dendritic epidermal T cell (DETC) line AU16 induce specific immunologic tolerance in vivo and inhibit the proliferation of native T cells in response to hapten-bearing dendritic cells in vitro. The purpose of this study was to test the hypothesis that these activities of DETC are mediated by a cytotoxic mechanism. In addition, because AU16 cells, unlike most DETC, express a TCR-alpha beta, we compared their activity in the in vivo and in vitro assays with a TCR(+)-gamma delta DETC line (T245) and an TCR(+)-alpha beta, FITC-specific T cell line (T4/28). Hapten-conjugated AU16 and T245 cells, but not T4/28 cells, induced tolerance to FITC in vivo. In addition, the proliferative response of naive T lymphocytes to gamma-irradiated, hapten-bearing APCs was inhibited by the addition of gamma-irradiated, FITC-conjugated DETC to the cultures on day 0. To determine whether the T cell or the APC was the target, AU16 cells were added to the cultures on day 4, when few APCs remained. FITC-conjugated AU16 and T245 cells profoundly inhibited [3H]thymidine incorporation by the T cells, indicating that the T cell was the target of the DETC. Furthermore, AU16 cells reduced the number of T cells in the in vitro proliferation assay, suggesting that inhibition of [3H]thymidine incorporation was a result of the cytotoxic activity of DETC. We speculate that cytotoxicity may also account for the ability of DETC to induce tolerance in vivo.
Animals↗
Effect of sunscreens on UV radiation-induced enhancement of melanoma growth in mice.
BACKGROUND: Epidemiologic evidence suggests that exposure to UV radiation plays a significant role in the development of melanoma skin cancers. As early surgical removal of the melanoma is the only effective therapy, current strategies for reducing mortality from melanoma focus on prevention of the disease. Chemical sunscreens protect mice from development of skin cancers that resemble sunlight-induced human squamous cell cancers, but there appears to be a complex relationship between UV radiation exposure and development of melanoma. PURPOSE: We asked whether common sunscreens would protect mice against UV radiation-induced enhancement of melanoma incidence. METHODS: C3H mice were exposed to 4.8 kJ/m2 UVB from FS40 sunlamps twice a week for 3 weeks. Sunscreens containing 7.5% 2-ethylhexyl-p-methoxycinnamate, 8% octyl-N-dimethyl-p-aminobenzoate, 6% benzophenone-3, or the oil-in-water vehicle alone were applied to the ears and tails of the mice 20 minutes before irradiation. At various times during and after exposure, we determined UV radiation-induced inflammation by measuring ear swelling. We also examined the ears histologically for UV radiation-induced alterations. One day after the final irradiation, 2.5 x 10(4) syngeneic K1735 melanoma cells were injected into the external ears. Mice were examined weekly for tumor growth for 5-8 weeks after tumor cell injection. Control mice were treated in the identical way except for exposure to UV radiation. RESULTS: The incidence of melanomas was significantly higher in the UV-irradiated mice. All three sunscreens protected against UV radiation-induced ear swelling and clearly diminished histopathologic alterations, including sunburn cell formation, epidermal hyperplasia, and mononuclear cell infiltrate in the dermis. However, the sunscreens failed to protect against UV radiation-induced increase in melanoma incidence. The sunscreens or vehicle alone did not significantly alter tumor growth. CONCLUSIONS: Protection against sunburn does not necessarily imply protection against other possible UV radiation effects, such as enhanced melanoma growth. IMPLICATIONS: Sunscreen protection against UV radiation-induced inflammation may encourage prolonged exposure to UV radiation and thus may actually increase the risk of melanoma development. These findings suggest that further research on the ability of sunscreens to prevent melanoma is urgently needed.
4-Aminobenzoic Acid↗
Inhibitory effect of a dendritic epidermal T cell line on K1735 melanoma cells in vivo and in vitro.
Murine epidermis contains a resident population of dendritic epidermal T cells (DETCs) with unknown function. We tested the ability of a cultured line of these cells to inhibit the growth of murine melanoma cells in vitro and in vivo. The interleukin-2 (IL-2)-dependent T cell line AU16, derived from the epidermis of C3H mice, was used as the source of DETCs. AU16 cells were cytotoxic to syngeneic K1735 and CM3205 C3H melanoma cell lines, as well as to a chemically induced cutaneous fibrosarcoma, in an in vitro 51Cr release assay. Mixing viable AU16 cells, but not splenic T cells, with K1735 melanoma cells immediately before intradermal injection into the flank of mice prevented or delayed the outgrowth of melanomas. AU16 cells killed by freezing and thawing and supernatants from cultures of AU16 cells did not inhibit melanoma growth in vivo or in vitro. Injection of viable AU16 cells intravenously or at a separate intradermal site had no effect on melanoma growth. These studies suggest that IL-2-activated DETCs have the potential to inhibit the growth of melanoma cells in vivo and that their cytotoxic activity may be responsible for this effect.
Animals↗
Ultraviolet irradiation of murine skin alters cluster formation between lymph node dendritic cells and specific T lymphocytes.
Exposure of murine skin to suberythemal doses of ultraviolet-B (UVB) radiation before contact sensitization alters the activity of antigen-presenting cells (APC) in the draining lymph nodes (DLN), decreases the contact hypersensitivity (CHS) response, and induces hapten-specific Ts cells. We determined whether in vivo UVB irradiation alters the ability of hapten-bearing APC from the DLN to form clusters with hapten-specific T lymphocytes. When APC from UV-irradiated, fluorescein isothiocyanate (FITC)-sensitized mice were mixed with a FITC-specific T-cell line, significantly fewer clusters formed compared with FITC+ APC from unirradiated mice. A higher percentage of clusters formed with APC from UV-irradiated mice were Mac-1+ and bound both CD4+ and CD8+ T cells, whereas FITC+ APC from nonirradiated mice bound CD4+ cells. These results suggest that UVB irradiation interferes with the induction of CHS by altering the functional interaction between APC and T cells, perhaps by altering the population of APC in the skin.
Animals↗
Enhanced development of murine melanoma in UV-irradiated skin: UV dose response, waveband dependence, and relation to inflammation.
Previously we reported that exposure of mice to UV radiation increases the incidence of melanomas arising from injection of syngeneic melanoma cells into the UV-irradiated ears. In this study, we investigated the UV dose-response characteristics, duration, waveband dependence, and role of inflammation in this effect of UV irradiation. The optimal conditions consisted of short term (3-4 weeks), intermittent (twice weekly) exposures to a moderate dose (4.8 kJ/m2) of UVB (280-320 nm) radiation from FS40 sunlamps and the effect lasted only for 3 days after the final UV irradiation. Removal of wavelengths below 315 nm with a Mylar filter abrogated the effect. The UV dose response and the time course of UV-induced inflammation, assessed by ear swelling and microscopic evaluation, did not correlate with that for enhanced melanoma outgrowth, nor did the treatment of the ears with the inflammatory agents turpentine and 12-o-tetradecanoyl phorbol-13-acetate mimic the UV effects on melanoma development. These results indicate that enhancement of melanoma development in UV-irradiated skin is probably unrelated to the inflammatory effects of UV irradiation.
Animals↗
Prevention of ultraviolet radiation-induced suppression of contact and delayed hypersensitivity by Aloe barbadensis gel extract.
We investigated the ability of Aloe barbadensis gel extract to prevent suppression of contact hypersensitivity (CHS) and delayed-type hypersensitivity (DTH) responses in mice by ultraviolet (UV) irradiation. Local immune suppression was induced in C3H mice by exposure to four daily doses of 400 J/m2 UV-B (280-320 nm) radiation from FS40 sunlamps, followed by sensitization with 0.5% fluorescein isothiocyanate (FITC) through the irradiated skin. Topical application of 0.167-1.67% Aloe gel after each irradiation significantly reduced this suppression. Aloe treatment partially preserved the number and morphology of Langerhans and Thy-1+ dendritic epidermal cells in skin, compared to those in the skin of mice given only UVR or UVR plus the vehicle. Experiments using a single (2 kJ/m2) dose of UVR followed by Aloe treatment showed that the effect of Aloe was not due to screening of the UVR. Systemic suppression of DTH to Candida albicans or CHS to FITC was induced in C3H mice exposed to 5 or 10 kJ/m2 UV-B radiation, respectively, on shaved dorsal skin and sensitized 3 d later with a subcutaneous injection of formalin-fixed Candida or FITC painted on unirradiated, ventral skin. Treatment of the UV-irradiated skin with Aloe immediately after irradiation prevented suppression of both DTH to Candida and CHS to FITC. Aloe treatment did not prevent the formation of cyclobutyl pyrimidine dimers in the DNA of UV-irradiated skin or accelerate the repair of these lesions. These studies demonstrate that topical application of Aloe barbadensis gel extract to the skin of UV-irradiated mice ameliorates UV-induced immune suppression by a mechanism that does not involve DNA damage or repair.
Adenosine Triphosphatases↗
Phenotypic and ultrastructural properties of antigen-presenting cells involved in contact sensitization of normal and UV-irradiated mice.
We investigated the surface phenotype and localization of hapten in antigen-presenting cells involved in the induction of contact hypersensitivity or tolerance. Dendritic cells collected 18 h earlier from the draining lymph nodes of mice sensitized with fluorescein isothiocyanate (FITC), which induce contact hypersensitivity upon injection into the foot-pads of naive mice, stimulated proliferation of lymphocytes from FITC-specific T-cell lines. By immunoelectron microscopy, these cells expressed high amounts of surface Ia molecules but had a negligible amount of FITC on the cell membrane. The majority of the FITC was localized in discrete structures in the cytoplasm, including mitochondria, endocytic vesicles, lysosomes, and cored tubules. In contrast, lymph node cells conjugated with FITC in vitro did not stimulate proliferation of FITC-specific T cells and showed a heavy, uniform distribution of FITC throughout the cytoplasm. Draining lymph node cells from mice exposed to ultraviolet (UV) radiation and then sensitized by applying FITC to the UV-irradiated skin, which induce tolerance upon injection into naive mice, induced significantly less proliferation of FITC-specific T cells than draining lymph node cells from unirradiated mice. The differences in activity of these cells, relative to draining lymph node cells from unirradiated, FITC-sensitized mice could not be attributed to a decreased number of Ia+ dendritic cells in the DLN, decreased surface expression of Ia molecules on these cells, or an alteration in the intracellular localization of hapten. However, a significantly higher percentage of the FITC+ dendritic cells from UV-irradiated mice expressed mac-1, -2, and -3 and F4/80 macrophage markers than did those from unirradiated animals, and fewer cells contained Birbeck granules, suggesting that a different population of Ia+ antigen-presenting cells may reach the draining lymph nodes of UV-irradiated mice.
Animals↗