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Pathogenesis of Leprosy

An Insight Into B Lymphocytes and Plasma Cells

Fabel, Agnes, MD*; Giovanna Brunasso, Alexandra Maria, MD; Schettini, Antonio Pedro, MD; Cota, Carlo, MD§; Puntoni, Matteo; Nunzi, Enrico, MD; Biondo, Giovanni, MD; Cerroni, Lorenzo, MD**; Massone, Cesare, MD

The American Journal of Dermatopathology: June 2019 - Volume 41 - Issue 6 - p 422–427
doi: 10.1097/DAD.0000000000001310
Original Study
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Abstract: The pathogenesis of leprosy is still not fully understood. Several studies have been performed on the involvement of T cells in leprosy and more recently have focused on genetic factors and innate immune response. There are still only few reports about the role of B cells in active leprosy lesions in different spectral forms of the disease. The literature on tuberculosis suggests that B cells play an important role in the regulation of the granulomas, in cytokine production, T-cell response, and antigen presentation. Only few studies investigated the role of B cell in leprosy. We investigated the distribution of B cells in 85 leprosy biopsies covering all forms of the disease and compared results with 13 biopsies of tuberculosis and atypical mycobacteriosis, expanding the previous experiences. A statistically significant difference in the number of CD20+ (P = 0.014) and CD138+ (P = 0.01) cells between the different forms of leprosy was observed. A remarkable amount of CD138+ cells could also be detected in borderline tuberculoid. The median of the CD20+ cells decreased from the bacilloscopy-negative samples to the bacilloscopy-positive samples by 50% (P = 0.004). Contrarily, the median of CD138+ cells showed an increase from bacilloscopy-negative to bacilloscopy-positive samples of 966.67% (P = 0.001). In our experience, tuberculoid leprosy showed more B cells and less plasma cells than lepromatous leprosy. Our results show that B cells might be implicated in leprosy pathogenesis, not only in the lepromatous pole as previously postulated, but also in tuberculoid granuloma formation and type 1 reactions.

*Neurological Centre Rosenhügel, Wien, Austria;

Dermatology Unit, Galliera Hospital, Genoa, Italy;

Fundação de Dermatologia Tropical Alfredo da Matta, Manaus, Brazil;

§San Gallicano Dermatological Institute, Rome, Italy;

Clinical Trial Unit, Scientific Directorate, E.O. Galliera Hospital, Genoa, Italy;

Centro di Riferimento Nazionale per il morbo di Hansen, San Martino University Hospital. Dr. Enrico Nunzi is now with the Department of Dermatology, Universitad Técnica Particular de Loja, Loja, Ecuador; and

**Research Unit Dermatopathology, Department of Dermatology, Medical University of Graz, Graz, Austria.

Correspondence: Cesare Massone, MD, Dermatology Unit, Ospedali Galliera, Via Volta 6, 16128 Genova, Italy (e-mail: cesare.massone@galliera.it).

The authors declare no conflicts of interest.

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