Leucine-rich glioma inactivated 3: a novel keratinocyte-derived melanogenic cytokine in vitiligo patients

Abstract

Background: In-vitro studies showed that Leucine-rich glioma inactivated 3 (LGI3) is a keratinocyte-derived cytokine that stimulates melanin synthesis and is increased after ultra violet B (UVB) irradiation. So, we postulated that LGI3 may be involved in vitiligo aetiopathogenesis and may participate in narrow band ultra violet B (NB-UVB) induced pigmentation in vitiligo. oBjectives: To assess this hypothesis, lesional LGI3 immunohistochemical expression of vitiligo patients before and after NB-UVB phototherapy was studied, and its correlation with repigmentation was evaluated. Methods: Forty vitiligo patients and 20 age, sex, and skin phenotype-matched controls were enrolled. Patients were treated with NB-UVB thrice weekly for 12 weeks. VASI score was evaluated before and after NB-UVB sessions. For vitiligo patients, baseline LGI3 immunohistochemical staining was estimated, and compared to that of controls and to its post-treatment data in those patients. Results: Baseline LGI3 immunohistochemical studied parameters (expression, intensity, percentage and H score) were significantly lower in vitiligo cases than controls (p=0.003, 0.013, 0.001 and 0.001 respectively). After 12 weeks of NB-UVB phototherapy, these LGI3 immunohistochemical parameters were up-regulated and became comparable to that of controls (p >0.05 for all). There was a significant positive correlation between the improvement of both VASI score and LGI3 H score mean values (r=-0.349 , p=0.027). study liMitations: Small number of investigated subjects. conclusions: Decreased LGI3 protein may play an active role in vitiligo pathogenesis and its up-regulation after NB-UVB phototherapy, may actively participate in NB-UVB photo-induced melanogenesis.

Livin is protective in UVB‐induced skin photodamage by regulating keratinocyte activation and inflammatory responses

“…Among these cytokines, TNF‐α, once released by KCs, can potentially trigger neighbouring KCs to enhance their responses. Upon binding with their respective receptors, these cytokines can activate NF‐κB, thereby regulating downstream gene expression 21 . At the same time, these cytokines can heighten the reaction of skin cells to UV radiation.…”

“…Upon binding with their respective receptors, these cytokines can activate NF-κB, thereby regulating downstream gene expression. 21 At the same time, these cytokines can heighten the reaction of skin cells to UV radiation. Inhibiting NF-κB can diminish the release of cytokines, which serves as a protective measure against UV radiation-induced skin damage.…”

Evaluation of the Langerhans cells role in vitiligo and its relationship to NB‐UVB

“…Genital organs were shielded, and eyes were covered during treatment. 11 Response to therapy was estimated clinically by observing the changes in color of the vitiliginous patches, 1 (no response, milky white color still present or erythematous color change), 2 (dull white color change), 3(Light brown color change), and 4 (Normal skin color). 12 For statistical purpose, cases achieving scores 2, 3, and 4 were lumped together and designated as responding versus score 1 as nonresponding.…”

“…At that time, irradiation was restarted at a dose lower than 20% and the dose was increased by 10% on subsequent sessions. Genital organs were shielded, and eyes were covered during treatment 11 …”