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UVB-NB Therapy

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What is
UVB-NB Therapy?

A potential advance in UVB-based phototherapy has been the introduction of fluorescent bulbs (Phillips model TL-01) that deliver UVB in the range of 310 to 315 nm, with a peak at 312 nm. It has a relatively narrow spectrum of emission which when compared with the older broad band UVB source has a reduction in erythemogenic wavelengths in the 290-305 nm range and 5-6 fold increased emission of the longer UVB wavelengths, thereby resulting in a higher phototherapy index for psoriasis.

Mechanism of action

In the skin, NB-UVB radiation is absorbed by DNA and urocanic acid and alters antigen presenting cell activity. NB-UVB is about 5-10 fold less potent than broad band UVB for erythema induction, hyperplasia, edema, sunburn cell formation and Langerhans cell depletion from the skin. It has a relatively more suppressive effect than broad band UVB on systemic immune responses as judged by natural killer cell activity, lymphoproliferation and cytokine responses.[8] The mechanism of action of NB-UVB phototherapy has not been completely understood. In psoriatics, NB-UVB phototherapy lowers peripheral natural killer cell activity, lymphocyte proliferation and immune regulatory cytokine production by both Th1 (IL-2, IFN-g) and Th2 (IL-10) T-cell populations.[8],[9]
Similar to PUVA therapy, NB-UVB may exert its effects in vitiligo in a two-step process. Both steps may occur simultaneously, the first being the stabilization of the depigmenting process and the second, the stimulation of residual follicular melanocytes.[10],[11] The well-documented immunomodulating effects of UV radiation can explain the stabilization of the local and systemic abnormal immune responses.[12] It is also likely that NB-UVB, similar to PUVA therapy, stimulates the dopa-negative, amelanotic melanocytes in the outer hair “root sheaths, which are activated to proliferate,” produce melanin and migrate outward to adjacent depigmented skin resulting in perifollicular repigmentation.[11] The ability of NB-UVB radiation to systemically suppress the major components of cell mediated immune function is thus likely to be linked to its beneficial effect in several inflammatory skin diseases including psoriasis.