Vol. 2 Issue 1 Part F

Introduction: Leprosy is one of chronic granulomatous disease that is caused by Mycobacterium leprae. This bacillus has a high affinity for skin and peripheral nerve cells. The clinical evolution of disease is determined by immune status of patients. Dendritic cells are one of the antigen-presenting cells (APCs) that play important role in initiating immune response to this pathogen. Langerhans cells and dermal dendrocytes are skin dendritic cells. These cells can be identified by using immunohistochemical markers such as CD1a and S-100.

Aim: To quantify the Langerhans cells and dermal dendrocytes by using immunohistochemical markers CD1a and S-100 in different forms of leprosy and to investigate the possible role of these denditic cells in the pathogenesis of the disease.

Methods: In the present study, 30 skin samples from patients with tuberculoid (19 biopsies) and lepromatous (11biopsies) leprosy were analyzed by using antibodies against CD1a and S-100.

Results: CD1a immunostaining: The mean number of positive Langerhans cells was 3.4 ± 0.7 cells/hpf in tuberculoid leprosy (TT) and was 0.4 ± 0.5cells/hpf in lepromatous leprosy (LL). Dermal dendrocytes were also on higher side in TT with mean value of 7.3± 03.15 and mean value of 0.3± 0.5 cells in LL. (statistically significant, p=0.001). S-100 immunostaining: The mean number of positive Langerhans cells was 2.8 ± 0.7 cells/hpf in TT cases and was 0.6± 0.3 in LL. The mean value of positive dermal dendrocytes was 12.6±6.5 cells in TT and 1.5± 2.3cells in LL. (statistically significant, p=0.001). No significant difference was seen in Langerhans cell and dermal dendrocytes number between TT and BT and between LL and BL histological subtypes on CD1a and S-100 immunostaining.

Conclusion: Quantitative analysis showed a clear predominanace of Langerhans cells and dermal dendrocytes in tuberculoid cases as compared to lepromatous cases. This indicates a role for dendritic cells in the cutaneous immune response and clinical evolution of leprosy.