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PubMed1993

Digestion of damaged DNA by the T7 DNA polymerase-exonuclease.

We have investigated the 3'-5'-exonuclease activity of phage T7 DNA polymerase for its usefulness as an approach for the detection of lesions in DNA. Unlike the T4 DNA polymerase-exonuclease, which is commonly used to map the position and frequency of lesions in very small DNA fragments, T7 DNA polymerase-exonuclease is able to hydrolyse almost completely the large fragments from KpnI-restricted mammalian DNA. However, we found that the exonuclease was also able to hydrolyse DNA containing several kinds of lesions: cyclobutane pyrimidine dimers, thymine glycols, and mono-adducts of 4'-hydroxymethyl-4,5',8-trimethylpsoralen and 5'-methyl-isopsoralen. Modifications of the reaction conditions did not significantly alter the extent of hydrolysis. These properties distinguish the T7 DNA polymerase-exonuclease from the T4 DNA polymerase-exonuclease and make the T7 DNA polymerase-exonuclease unsuitable for detecting several types of lesions in DNA.

Animals↗
PubMed2001

Ultraviolet exposure as the main initiator of p53 mutations in basal cell carcinomas from psoralen and ultraviolet A-treated patients with psoriasis.

Basal cell carcinoma, the most frequent skin cancer in humans, is often linked to chronic sun exposure. In psoralen and ultraviolet A-treated psoriatic patients, basal cell carcinomas may occur even more frequently; however, the exact etiology and mechanisms of tumorigenesis in psoriatic patients are unclear because psoralen and ultraviolet A is not only a carcinogen but also an immunosuppressor and because psoralen and ultraviolet A-treated psoriatic patients often have other (co)carcinogenic risk factors (e.g, therapeutic exposure to ultraviolet B, X-ray radiation, arsenic, tar, and/or chemotherapeutic agents such as methotrexate). In this study, we analyzed the DNA of 13 basal cell carcinomas from five psoralen and ultraviolet A-treated psoriatic patients for mutations of the p53 tumor suppressor gene. DNA sequencing revealed a total of 11 mis-sense, two non-sense, and four silent mutations in seven of the 13 basal cell carcinomas (54%). Of the 13 total mis-sense or non-sense mutations, 12 (92%) occurred at dipyrimidine sites and nine (69%) were of the ultraviolet fingerprint type (eight C-->T transitions and one CC-->TT transition). Three of the C-->T transitions occurred at dipyrimidine sites opposite a 5'-TpG sequence (a potential psoralen-binding site and target for psoralen and ultraviolet A mutagenesis). Thus, whether these mutations were induced by ultraviolet or psoralen and ultraviolet A was not clear. In addition, two other mutations (15%) occurred at 5'-TpG sites, one (8%) occurred at a 5'-TpA site (the most frequent site of psoralen binding and mutagenesis in cell and murine studies), and one (8%) involved a G-->T transversion. These results suggest that (i) the major initiator of p53 mutations in basal cell carcinoma in psoralen and ultraviolet A-treated psoriasis patients is environmental and/or therapeutic ultraviolet(B) exposure, and that (ii) psoralen and ultraviolet A itself causes only a smaller portion of p53 mutations in psoralen and ultraviolet A-associated basal cell carcinomas.

Adult↗
PubMed2004

The ultraviolet fingerprint dominates the mutational spectrum of the p53 and Ha-ras genes in psoralen + ultraviolet A keratoses from psoriasis patients.

Psoriasis patients exposed to high cumulative doses of psoralen + ultraviolet A frequently exhibit so-called "psoralen + ultraviolet A keratoses" (i.e., hyperkeratotic lesions with varying degrees of histologic atypia). The exact causes and molecular mechanisms of psoralen + ultraviolet A keratoses however, are not clear. We therefore performed DNA mutational analysis of the tumor suppressor gene p53 (exons in psoralen + ultraviolet A keratoses from 10 long-term psoralen + ultraviolet A-treated psoriasis patients. We detected 39 p53 mutations in 16 of 28 psoralen + ultraviolet A keratoses (57%) and 18 Ha-ras mutations in 11 of 25 psoralen + ultraviolet A keratoses (44%). Of the 39 p53 mutations and 18 Ha-ras mutations, 22 (56%) and 13 (72%), respectively, were of the ultraviolet fingerprint type (C-->T or CC-->TT transitions at dipyrimidine sites); 13 (33%) and two (11%), respectively, occurred at potential psoralen-binding sites (5'-TpA, 5'-TpG, or 5'-TpT DNA sequences) and were potentially psoralen + ultraviolet A induced; two (5%) and three (17%), respectively, were of ambiguous origin (ultraviolet and/or psoralen + ultraviolet A); and two (5%) and none (0%), respectively, were of the "other" type, respectively. We conclude that (1) the frequent mutation of p53 and Ha-ras may play a key part in the formation of at least some psoralen + ultraviolet A keratoses; (2) environmental and/or therapeutic ultraviolet exposure may be a major cause of psoralen + ultraviolet A keratosis as most Ha-ras and p53 mutations are induced by ultraviolet light; and (3) psoralen + ultraviolet A itself plays a smaller, though direct, role in causing these mutations.

Adult↗
PubMed2003

A randomized controlled trial of narrowband ultraviolet B vs bath-psoralen plus ultraviolet A photochemotherapy for psoriasis.

BACKGROUND: In 1991, consensus guidelines recommended psoralen plus ultraviolet A photochemotherapy (PUVA) for those requiring second-line therapy for psoriasis. Narrowband (TL-01) UVB has since become more widely available, replacing the less effective broadband sources. Objectives To compare the efficacy of TL-01 UVB phototherapy and trimethoxypsoralen (TMP) bath-PUVA for chronic plaque psoriasis. PARTICIPANTS AND METHODS: A randomized, observer-masked, intraindividually controlled, paired (half-body) study was done in the Photo(chemo)therapy Unit in Ninewells Hospital and Medical School, Dundee. The study comprised 28 patients (skin phototypes I-III) with chronic plaque psoriasis. Each patient's body halves (sagittal plane) were treated independently, one-half with TL-01 UVB, the other with bath-PUVA. Both treatments were administered according to standard, optimized regimens. Treatment was continued until clearance or minimal residual activity (MRA), or a maximum of 30 treatments. The main outcome measures were treatments and time to clearance/MRA, the proportion reaching clearance/MRA, change in psoriasis severity score (scaling, erythema and induration) and remission durations. RESULTS: Of 18 who completed the study, all reached clearance/MRA with TL-01, but three were still not clear after 30 PUVA exposures. TL-01 achieved clearance/MRA a median of 11 (6.5-25; P = 0.001) days more quickly than PUVA, but required a median of 24.5 compared with 19 exposures [95% confidence interval (CI) for difference 1.5-5.5; P = 0.01]. Ten patients were withdrawn (four because of inadequate response of PUVA-treated halves). Analysed on an intention-to-treat basis, 21 of 28 (75%) of all participants reached clearance/MRA with TL-01 compared with 15 of 28 (54%) with PUVA (95% CI for difference 4-37%; P = 0.03). Remission durations did not differ. CONCLUSIONS: When administered according to these regimens in a skin phototype I-III population, TL-01 UVB is more efficacious than TMP bath-PUVA in the treatment of chronic plaque psoriasis.

Adult↗
PubMed2002

Psoralen photochemotherapy (PUVA) is only moderately effective in widespread vitiligo: a 10-year retrospective study.

A 10-year retrospective analysis of the use of psoralen photochemotherapy (PUVA) in the treatment of vitiligo was undertaken at the St John's Institute of Dermatology, London, UK. Of 97 patients included in this study, eight had complete or almost complete repigmentation, 59 moderate to extensive repigmentation, and 30 showed little or no response. However, 24 of those who had responded to PUVA with extensive repigmentation did not consider their response satisfactory because of persistence of vitiligo at cosmetically sensitive sites, and poorly matching, speckled repigmentation. Fifty-seven patients who initially improved with PUVA therapy subsequently relapsed, in most cases within a year of stopping treatment. Relapses in 22 patients were on the same cutaneous sites as previously affected, while vitiligo at new sites developed in 20 patients and both new and old sites were affected in a further 15 patients. Patients who retained their pigmentation after 2 years appeared to have a better chance of permanent remission. The only statistically significant prognostic indicator of relapse was patient age at the start of treatment, younger patients tending to retain their pigmentation longer than older patients. This study emphasizes the need for careful patient counselling before PUVA therapy as this treatment seldom achieves extensive repigmentation that is cosmetically acceptable, and treatment response is often followed by relapse.

Adult↗
PubMed2002

Amino acids in SRS1 and SRS6 are critical for furanocoumarin metabolism by CYP6B1v1, a cytochrome P450 monooxygenase.

CYP6B1v1 is the principal cytochrome P450 monooxygenase (P450) that detoxifies dietary furanocoumarins in the guts of Papilio polyxenes, the black swallowtail caterpillar. Sequence alignments and structure comparisons of CYP6B1v1 with the mouse CYP2A5 and bacterial CYP102 proteins, which are also capable of metabolizing the linear furanocoumarin xanthotoxin (8-methoxypsoralen), suggested that Phe116, His117, Val368 and Phe484 might be active site residues. In a homology model developed for CYP6B1v1, the side chains of Phe116 and His117 located in the B'-C loop of SRS1 are predicted to be positioned above the haem plane, while the side chain of Phe484 located in SRS6 is predicted near the entrance of the catalytic pocket. Site-directed mutagenesis of residues Phe116, His117 and Phe484 indicated that these residues represent several of those that determine this protein's stability and substrate specificity. Whereas all aromatic mutants of Phe116 and Phe484 generated CO-difference spectra with maxima at 450 nm indicative of correctly configured monooxygenases, aromatic mutants of Phe116 exhibited reduced reactivities toward some furanocoumarins and aromatic mutants of Phe484 eliminated all reactivities toward furanocoumarins. All single and double aliphatic mutants of Phe116, His117 and Phe484 and aromatic mutants of His117 generated carbon monoxide (CO) difference spectra with maxima at 420 nm (P420) indicative of incorrectly configured monooxygenases. These studies define residues Phe116, His117 and Phe484 as determinants of this insect P450's catalytic site integrity and residues Phe116 and Phe484 as determinants of its substrate specificity. Conservation of Phe116 and His117 in an array of lepidopteran CYP6B proteins implies that these amino acids serve a similar function in other monooxygenases of the insect CYP6B subfamily.

5-Methoxypsoralen↗
PubMed2000

Psoralen-ultraviolet A therapy vs. psoralen-ultraviolet B therapy in the treatment of plaque-type psoriasis: our experience with fitzpatrick skin type IV.

BACKGROUND: Oral psoralen, when combined with UVB, shows an increased response in psoriasis. In this study, conventional psoralen-UVA (PUVA) therapy was compared with psoralen-UVB (PUVB) therapy in plaque-type psoriasis in patients with Fitzpatrick skin type IV. PATIENTS AND METHODS: Equal numbers of patients with stable, plaque-type psoriasis were treated with either PUVA (n = 22) or PUVB (n = 22), three times weekly until 90% clearance was achieved. A final evaluation was made 3 months later. RESULTS: The two groups showed no significant differences in terms of clearance of disease, mean number of exposures, or the average duration of therapy; however, the cumulative dose of UVB required for clearance was significantly lower than that of UVA. Both groups had a similar acute side-effects' profile. CONCLUSIONS: PUVB therapy is as effective as conventional PUVA in the treatment of stable, plaque-type psoriasis in patients with Fitzpatrick skin type IV. A significantly lower dose of UVB is required for clearance as compared with UVA.

Adult↗
PubMed2001

Bullous lesions in Bazex syndrome and successful treatment with oral psoralen phototherapy.

A 59-year-old man presented with a psoriasiform dermatitis with associated bullae and destructive nail dystrophy of the hands and feet. He had lost 10 kg weight over 6 months and a mass in the neck was noted. He was provisionally diagnosed with Bazex syndrome (acrokeratosis paraneoplastica) and subsequent investigations revealed a squamous cell carcinoma in the right piriform fossa. His skin lesions were treated with oral psoralen and ultraviolet A phototherapy and this cleared the cutaneous changes, but the nail changes have persisted at 18 months follow up.

Acrodermatitis↗
PubMed1998

A novel in vivo model for evaluating agents that protect against ultraviolet A-induced photoaging.

Increasing evidence demonstrates that ultraviolet A radiation (UVA) contributes to photoaging, which results in the accumulation of massive amounts of abnormal elastic material in the dermis of photoaged skin. To study UVA-induced photoaging in an in vivo system, we utilized a line of transgenic mice containing the human elastin promoter linked to a chloramphenicol acetyl transferase reporter gene. Our prior work demonstrates promoter activation in response to ultraviolet B radiation (UVB), UVA, and psoralen plus ultraviolet A radiation in the skin of these mice. The addition of psoralen (8-MOP) prior to administration of UVA results in substantial increases in promoter activation, as compared with UVA alone. To demonstrate the utility of these mice as a model of UVA-induced photodamage, we administered four lotions to the skin of our transgenic mice that included: a sunscreen containing octyl methoxycinnamate and benzophenone-3 with a sun protection factor (SPF) of 15, the UVA filter butyl methoxydibenzoylmethane, the SPF 15 sunscreen and the UVA filter together, and the lotion vehicle alone. Following sunscreen administration, mice received a single psoralen plus ultraviolet A radiation treatment. All sunscreens decreased chloramphenicol acetyl transferase activity with the SPF 15 sunscreen, the UVA filter, and the combination SPF 15 sunscreen and UVA filter, resulting in increasing degrees of protection against psoralen plus ultraviolet A radiation. These results demonstrate that this model functions as a rapid and sensitive model of UVA photodamage for the identification and comparison of compounds that protect against UVA-induced photoaging.

Animals↗
PubMed2002

Incidence and risk factors associated with a second squamous cell carcinoma or basal cell carcinoma in psoralen + ultraviolet a light-treated psoriasis patients.

Psoralen + ultraviolet A-treated psoriasis patients are at increased risk for squamous cell carcinomas and basal cell carcinomas; however, the incidence and risk factors associated with second squamous cell carcinomas and basal cell carcinomas in this population are not well qualified. Incidence and risk factors for second squamous cell carcinomas and basal cell carcinomas were studied in a cohort of 1380 psoralen + ultraviolet A-treated psoriasis patients prospectively followed for over 20 y; 264 had a squamous cell carcinoma and 258 a basal cell carcinoma after beginning psoralen + ultraviolet A therapy. After a first squamous cell carcinoma, the risk of a second squamous cell carcinoma was 26% at 1 y, 62% at 5 y, and 75% at 10 y. Risk increased with high psoralen + ultraviolet A exposure prior to the first squamous cell carcinoma (hazard ratio 3.32, 95% confidence interval 1.53, 7.18). Higher rates of post-first squamous cell carcinoma psoralen + ultraviolet A treatment also were associated with greater risk (hazard ratio 1.56 for every additional 10 treatments per year for patients with low pre-first squamous cell carcinoma psoralen + ultraviolet A exposure, 95% confidence interval 1.35, 1.81). Patients exposed to high levels of tar and/or ultraviolet B before a first squamous cell carcinoma were also at higher risk (hazard ratio 1.72, 95% confidence interval 1.14-2.60). Risk of a second basal cell carcinoma was 21% at 1 y, 49% at 5 y, and 61% at 10 y. There was some evidence that high exposure to psoralen + ultraviolet A before a first basal cell carcinoma was associated with increased risk of second basal cell carcinoma (hazard ratio 1.45, 95% confidence interval 0.97-2.17). Higher post-first tumor psoralen + ultraviolet A treatment rates also increased risk (hazard ratio 1.24 for every additional 10 treatments per year, 95% confidence interval 1.06-1.47). Psoralen + ultraviolet A-treated psoriasis patients appear to have a greatly increased incidence of second squamous cell carcinoma compared with the general population. Patients who develop a squamous cell carcinoma after starting psoralen + ultraviolet A therapy should be closely monitored for a subsequent squamous cell carcinoma.

Aged↗
PubMed2003

High frequency of ultraviolet mutations at the INK4a-ARF locus in squamous cell carcinomas from psoralen-plus-ultraviolet-A-treated psoriasis patients.

Squamous cell carcinomas in psoralen-plus-ultraviolet A (PUVA) treated patients frequently exhibit p53 tumor suppressor genes and Ha-ras protooncogenes that are mutated at dipyrimidine sites and carry the ultraviolet fingerprint (i.e., C-to-T or CC-to-TT transitions). To further broaden the knowledge of genetic mutations in PUVA-associated skin cancer, we used DNA sequencing analysis to study the mutational spectrum of the INK4a-ARF locus in 26 squamous cell carcinomas from 11 long-term PUVA-treated psoriasis patients and classified the mutations by origin (ultraviolet, ultraviolet and/or PUVA, or other). Nineteen INK4a-ARF missense/nonsense mutations were found in exons 1alpha, 1beta, and 2 in 11 of 26 squamous cell carcinomas (42%) from seven of 11 patients (64%). Eleven mutations (58%) were of the ultraviolet type; three (16%) were of the ultraviolet and/or PUVA type (i.e., C-to-T transitions at dipyrimidine sites opposite a 5'TpG sequence, a potential psoralen binding site); and five (26%) were of other type. Interestingly, 10 of 11 patients (91%) showed intron polymorphism C500G at the 3' untranslated region of exon 3. These data indicate that (i) INK4a-ARF mutations frequently occur in PUVA-associated squamous cell carcinomas; (ii) ultraviolet B radiation is the major cause of these mutations; and (iii) PUVA itself may play no direct role in development of most INK4a-ARF mutations.

Adult↗
PubMed2003

Correlations between clinical, histologic, blood, and skin polymerase chain reaction outcome in patients treated for mycosis fungoides.

Little information is currently available regarding post-treatment outcome of TCR-targeted PCR in skin and/or peripheral blood in patients with Mycosis Fungoides (MF) when a dominant gene rearrangement is present at time of diagnosis. To address this matter, a study evaluating the correlations between post-treatment clinical, histological, blood and skin PCR data was conducted in MF patients. Twenty-seven MF patients with dominant gene rearrangement in skin lesions at time of diagnosis were selected. Peripheral blood samples were investigated as well before treatment and post treatment molecular data in skin and blood were compared with clinical and histological outcome. A dominant gene rearrangement was detected before treatment in blood of 16/25 patients. The dominant gene rearrangement disappeared from cutaneous lesions in 8/13 patients displaying complete clinical and histological response whereas skin PCR remained positive in all 10 patients with histologically persistent disease. A dominant gene rearrangement was still present in blood in 10/16 patients after treatment and blood data were not correlated with skin molecular response. This study confirms frequent detection of a dominant gene rearrangement in peripheral blood in MF patients and shows that PCR may remain positive in lesional sites even when skin lesions are successfully treated.

Adult↗
PubMedDate not supplied

Hypopigmented mycosis fungoides in childhood and adolescence.

We present a case of purely hypopigmented mycosis fungoides of 8-years duration in an 18-year-old woman who responded readily to psoralen plus ultraviolet A (PUVA) treatment. The literature pertaining to hypopigmented mycosis fungoides is reviewed.

Adolescent↗
PubMed1997

Psoralen-mediated photodecontamination of platelet concentrates: inactivation of cell-free and cell-associated forms of human immunodeficiency virus and assessment of platelet function in vivo.

BACKGROUND: Treatment of platelet concentrates (PCs) with psoralens and broad-band ultraviolet A (UVA) radiation is being examined for the elimination of pathogens that might be present in donated blood. Previous studies have demonstrated the inactivation of cell-free viruses and the maintenance of platelet integrity with common in vitro assays. STUDY DESIGN AND METHODS: Human immunodeficiency virus (HIV) in three forms-cell-free, activity replicating, and latently infected cell lines-was added to PCs and treated with 50-microgram per mL of 4'-aminomethyl-4,5',8-trimethylpsoralen (AMT), 0.35 mM rutin, and broad- and narrow-band UVA light (320-400 nm and 360-370 nm [UVA1], respectively). The inactivation of added HIV was assessed in tissue culture; platelet hemostatic activity was assessed in thrombocytopenic rabbits. RESULTS: Each form of HIV was inactivated completely (> or = 10(5) infectious units) on treatment with 30 J per cm2 of UVA1 light. Similar results were obtained on treatment of 2.5 mL of PCs in test tubes or intact PC units (50 mL) in blood bags. Latently infected cell lines were substantially more sensitive than cell-free HIV or HIV that was actively replicating. Human platelets treated with 40 J per cm2 of UVA1 light had a fully corrected bleeding time shortly after treatment or after 5 days' storage, as assessed in thrombocytopenic rabbits. Platelet hemostatic function began to decrease with 81 J per cm2 of UVA1 light and was abolished with 113 J per cm2. At similar fluences, broad-band UVA light was more injurious to platelets than was UVA1 light. CONCLUSION: HIV transmission might be eliminated by PCs after treatment with AMT and UVA1 light and without a reduction in platelet hemostatic function.

Animals↗
PubMed1999

Elimination of cytokine production in stored platelet concentrate aliquots by photochemical treatment with psoralen plus ultraviolet A light.

BACKGROUND: Cytokines generated in platelet concentrates (PCs) during storage have been implicated as possible mediators of febrile nonhemolytic transfusion reactions. Two potential methods of white cell inactivation were compared for their ability to reduce cytokine synthesis in pooled random-donor PC aliquots: treatment with gamma-radiation and photochemical treatment (PCT) using psoralens and ultraviolet A light. STUDY DESIGN AND METHODS: ABO-matched PC aliquots were pooled and divided into separate aliquots. Aliquots (20 mL) were taken from each pool to serve as an untreated control and to undergo gamma-radiation. Aliquots were treated by using either gamma-radiation (2500 or 5000 cGy) or virucidal PCT. PCT with the psoralens 8-methoxypsoralen (8-MOP), aminomethyltrimethyl psoralen (AMT), and S-59 was investigated. PC aliquots were stored for 7 days and analyzed for levels of interleukin 8 by use of an enzyme-linked immunosorbent assay. Levels of DNA adduct formation were determined by using 3H-labeled psoralens. RESULTS: Levels of interleukin 8 in the untreated random-donor PC aliquots increased with increasing white cell counts, but they were not affected by pooling. The untreated control aliquots and the aliquots treated with gamma-radiation had significant increases in levels of interleukin 8 after 5 to 7 days of storage (p<0.05). PCT with S-59 resulted in a significant reduction in cytokine synthesis (p<0.05). Day 5 to 7 levels of interleukin 8 did not differ significantly from Day 0 levels. Inhibition of interleukin 8 production by PCT increased with increasing levels of DNA modification (S-59 > AMT > 8-MOP). CONCLUSION: PCT that utilizes S-59 has been developed to inactivate potential viral and bacterial pathogens in PC aliquots while maintaining in vitro platelet function. These data demonstrate that PCT of aliquots of pooled PC aliquots before storage also prevents white cell cytokine synthesis during storage. PCT may therefore offer the potential for reducing cytokine-associated febrile nonhemolytic transfusion reactions.

Blood Preservation↗
PubMed2000

Assessment of donor T-cell function in cellular blood components by the CD69 induction assay: effects of storage, gamma radiation, and photochemical treatment.

BACKGROUND: Functional donor T-lymphocytes in blood components may cause a variety of transfusion complications. A flow cytometric assay based on the measurement of induced CD69 expression may be an alternative to cell proliferation methods in determining the functional status of these cells in blood components. STUDY DESIGN AND METHODS: Seven units of whole blood, RBCs, and platelet concentrates (PCs) were stored under blood bank conditions. Half of 3 PCs each were gamma-radiated or treated with UVA+psoralen; the other half served as controls. Samples were analyzed for phorbolester-induced expression of CD69 as an indicator of cell responsiveness and for exclusion of propidium iodide as a measure of cell membrane integrity and viability. RESULTS: CD69 inducibility and propidium iodide exclusion decreased exponentially (half-life, 3. 3 and 8.1 days, respectively) during cold blood storage. Irradiation and UVA+psoralen treatment of PCs immediately reduced CD69 inducibility to 21 percent (controls, 82%; p = 0.004) and 12 percent (controls, 95%; p = 0.0008), respectively. The proportion of cells capable of propidium iodide exclusion was similar in treated samples and controls, but it declined faster in the treated samples during subsequent storage. CONCLUSION: Flow cytometric measurement of CD69 induction can be adapted to provide quantitative assessment of T-cell function in blood components. Results obtained by the CD69 assay are in general agreement with those previously reported by use of proliferation methods; the assay may be useful for special applications in transfusion medicine.

Antigens, CD↗
PubMed2003

The effect of exposing murine splenocytes to UVB light, psoralen plus UVA light, or gamma-irradiation on in vitro and in vivo immune responses.

BACKGROUND: WBCs in blood components are a major factor contributing to immune responses such as GVHD and alloimmunization that follow transfusion. Irradiation of blood components has been used to regulate the contribution of donor WBCs to these immune responses. A systematic comparison of how the exposure of lymphoid cells to gamma-irradiation, UVB light, or psoralen + UVA light (PUVA) effects immune response was conducted to better define the best type of irradiation to be used in different clinical settings. STUDY DESIGN AND METHODS: Murine spleen cells were irradiated with varying doses and tested for their in vitro ability to be activated, to proliferate in response to mitogen or allogeneic stimulator cells, or to serve as stimulator cells. Irradiated donor cells were also tested for in vivo generation of GVHD, induction of alloantibody production, induction of restricted cytolytic T lymphocytes, and persistence of irradiated cells. RESULTS: In general, increasing amounts of irradiation resulted in increased inhibition of in vitro and in vivo responses, although the doses required for inhibition differed from assay to assay. In contrast, irradiation of donor cells did not always result in inhibition of recipient alloantibody responses but was dependent on the donor-recipient combination that was studied. CONCLUSION: Control of the in vivo outcomes of transfusing allogeneic cells is regulated by the type and dose of irradiation used and by the genotype of the donor and/or recipient.

Animals↗