How does PUVA inhibit delayed cutaneous hypersensitivity?

Moss, Celia; Friedmann, Peter S.; Shuster, Sam

doi:10.1111/j.1365-2133.1982.tb00400.x

Cited by 21 publications

(3 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has already been reported that PUVA therapy downregulates the immune response both in vivo (2)(3)(4)(5)(6)(8)(9)(10) and in vitro (7). We demonstrated here that PUVA therapy not only downregulates T-cell function but also suppresses the expression of cell adhesion molecules of T lymphocytes in vitro.…”

Section: Discussionsupporting

confidence: 62%

“…On the other hand, effects of PUVA therapy on circulating lymphocytes have also been indicated; namely, reduction in the numbers of circulating Erosette-forming lymphocytes (2), improvement of T-cell levels assessed by E-rosettes (3,4) and reduction in the number of circulating helper/inducer T cells (OKT4) (5). PUVA also inhibits DNA synthesis of circulating lymphocytes in vivo (6), and reduces cell-mediated immune responses (7) and delayed cutaneous hypersensitivity (2,(8)(9)(10). UVA light can reach the superficial part of the dermis by penetrating the epidermis (11).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

PUVA suppresses the expression of cell adhesion molecules of lymphocytes

Urano

Matsuyama

Urano

et al. 1995

Experimental Dermatology

View full text Add to dashboard Cite

To determine the therapeutic mechanism of PUVA in psoriasis vulgaris, the effects of PUVA on activated T lymphocytes were investigated in vitro. Peripheral blood mononuclear cells (PBMC) obtained from healthy volunteers were activated with Con A stimulation (Con A blasts). Both untreated PBMC and Con A blasts were irradiated with UVA light in the presence of 8-methoxypsoralen (8-MOP). The expressions of CD4, CD8, VLA-4 and LFA-1 of PBMC and Con A blasts were stained with each monoclonal antibody and the intensity of fluorescence was analyzed by FACScan. PUVA-treated PBMC showed decreased response to both Con A and PHA stimulation. PUVA treatment also suppressed the IL-2 production of Con A blasts and IL-2 response of PBMC with increasing UVA fluence. The expressions of LFA-1, VLA-4, CD4, CD8 and CD25 (IL-2R) molecules were decreased in PUVA-treated Con A blasts. Con A blasts were more sensitive than untreated PBMC to PUVA treatment. These results suggest that the therapeutic effects of PUVA on psoriasis vulgaris can be induced by suppression of the expression of cell surface molecules of activated T lymphocytes.

show abstract

Section: Discussionsupporting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

PUVA suppresses the expression of cell adhesion molecules of lymphocytes

Urano

Matsuyama

Urano

et al. 1995

Experimental Dermatology

View full text Add to dashboard Cite

show abstract

“…A course of psoralen-UVA (PUVA) treatment given for psoriasis caused substantially greater suppression of the sensitization phase of DNCB than of the elicitation phase (Moss et al, 1982). Previously, no human studies have directly compared the effects of one exposure of UVR on sensitization and elicitation responses in the same CHS model.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Solar-Simulated Radiation on the Elicitation Phase of Contact Hypersensitivity does not Differ Between Controls and Patients with Polymorphic Light Eruption

Palmer

Hawk

Young

et al. 2005

Journal of Investigative Dermatology

View full text Add to dashboard Cite

It has been suggested that polymorphic light eruption (PLE) is characterized by a failure of ultraviolet radiation (UVR)-induced immunosuppression, resulting in a type-IV hypersensitivity response to photoinduced antigens. We measured the effect of solar-simulated radiation (SSR) on the elicitation phase of contact hypersensitivity to 2,4-dinitrochlorobenzene (DNCB), in ten PLE patients and 11 controls. Subjects were given a sensitizing dose of DNCB, and 3 wk later were exposed to 0.75 and 2 minimum erythema doses (MED) of SSR on the upper inner arm. Immediately and 24 h later these sites, and a non-irradiated control site, were challenged with DNCB. The resulting increase in skin thickness was measured with high-frequency ultrasound. Overall, 2 MED caused 17%-20% suppression of elicitation responses (compared with 93% suppression of sensitization reported previously), but the effect of SSR varied greatly between subjects, with some subjects showing potentiated responses, which may be of relevance to false-positive reactions in photopatch testing. In a repeated measures general linear model, SSR overall caused significant suppression of responses (p<0.001); there was less suppression in older subjects (p=0.009) but there was no significant difference between PLE patients and age-matched normal controls. These results contrast with our previous finding of a resistance to UVR-induced suppression of sensitization to DNCB in PLE. This difference may reflect the greater importance of Langerhans cells in the sensitization phase, and is consistent with the hypothesis that PLE arises from impaired suppression of Langerhans cell activation or migration.

show abstract

Mutagenicity and Carcinogenicity of Methoxsalen Plus UV-A

Roelandts¹

1984

Arch Dermatol

View full text Add to dashboard Cite

How does PUVA inhibit delayed cutaneous hypersensitivity?

Cited by 21 publications

References 14 publications

PUVA suppresses the expression of cell adhesion molecules of lymphocytes

PUVA suppresses the expression of cell adhesion molecules of lymphocytes

The Effect of Solar-Simulated Radiation on the Elicitation Phase of Contact Hypersensitivity does not Differ Between Controls and Patients with Polymorphic Light Eruption

Mutagenicity and Carcinogenicity of Methoxsalen Plus UV-A

Contact Info

Product

Resources

About