Do Langerhans Cells Have a Role in the Mechanism of Neuropathy?

Hayriye Külbay

Keywords: LCs, diabetes, neuropathy

Aim:

The causative mechanism for the neuropathy is still unclear. In this study it is hypothesized that LC characteristics might be altered in patients with diabetic neuropathy compared to a group of control subjects.

Method:

The density, cell body area, perimeter and the numbers of LCs in the epidermis of human skin were quantified; 25 specimens from 10 neuropathic patients and 28 specimens of 12 non-neuropathic healthy subjects which served as controls. Skin punch biopsies from six matching sites (glabrous and non-glabrous forearm, thigh, back, proximal and distal leg) were taken and tissues were processed for indirect immunofluorescence using anti-Langerin/CD 207 as primary antibody with an appropriate TRITC-conjugated secondary. Stained sections were scanned using confocal microscopy, and images quantitated using Neurolucida image analysis software. Statistical comparisons of the test groups’ cell counts, cell body areas, and cell perimeters were performed using Student’s t-test or analysis of variance.

Results:

LC density was found significantly higher in total samples in the patient group (449.4 cells/mm2) than in the control group (234.1 cells/mm2). Individual cell area, the number and perimeter of LCs were also significantly higher in the patient group; LC numbers (21.2 ± 1.1 cells/mm epidermis in patients; 15.3 ± 1.3 cells/mm in controls, p<0.03), cell body area (172.3 ± 12.3 µm² in patients; 37.5 ± 2.8 µm² in controls, p<0.0001) and perimeter (75.4 ± 2.6 µm in patients; 33.2 ± 2.1 µm in controls, p<0.0001). Additionally, LC processes were demonstrated deformed compared to controls.

Conclusions:

This study demonstrates that in diabetic neuropathy patients there are differences in LCs, suggesting that LCs could play a role in the pathogenesis of altered vasodilation and possibly generation or maintenance of neuropathy itself.

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