Immunohistochemical assessment of cell populations in leprosy-spectrum lesions and reactional forms
Luciana Raquel Vincenzi Fachin1, Cleverson Teixeira Soares2, Andrea de Faria Fernandes Belone1
1Laboratory of Anatomic Pathology, Instituto Lauro de Souza Lima, Bauru, São Paulo, Brazil.
Insights
Leprosy lesion immunophenotyping reveals distinct immune cell profiles across disease forms. Understanding these cellular differences, like T cell distribution and macrophage phenotypes, is key to leprosy pathogenesis.
Area of Science:
- Immunology
- Dermatology
- Pathology
Background:
- Leprosy exhibits diverse clinical and immunological manifestations.
- In situ immunophenotyping of leprosy lesions is crucial for understanding inflammatory cell roles in Mycobacterium leprae infection.
Purpose of the Study:
- To comprehensively analyze the in situ immunophenotype of inflammatory cells in various forms of leprosy.
- To correlate cellular profiles with disease classification and reactions.
Main Methods:
- Biopsies from healthy controls and leprosy patients (TT, BT, BB, BL, LL, R1, R2) were analyzed.
- Immunohistochemistry was used to detect CD3, CD4, CD8, FoxP3, CD20, CD138, CD1a, CD57, CD15, CD117, CD68, and CD163.
- Histochemistry identified eosinophils; macrophage phenotypes (M1/M2) were assessed.
Main Results:
- Higher CD3+ and CD4+ T cells in Tuberculoid (TT) vs. Lepromatous Leprosy (LL).
- CD8+ T cells were prominent in epidermal infiltrates.
- M1 macrophages in TT/R1 granulomas, M2 in LL granulomas.
- Decreased CD1a+ cells from TT to LL; increased neutrophils in Erythema Nodosum Leprosum (R2).
Conclusions:
- Distinct immune cell populations characterize different leprosy forms and reactions.
- Macrophage polarization (M1/M2) correlates with disease spectrum.
- All investigated cells, except eosinophils, contribute to leprosy immunopathogenesis.
Abstract:
In situ immunophenotyping of leprosy lesions can improve our understanding of the biology of inflammatory cells during the immune response to Mycobacterium leprae antigens. In the present study, biopsies from 10 healthy controls and 70 leprosy patients were selected, 10 for each of the following conditions: clinical tuberculoid (TT), borderline tuberculoid (BT), borderline borderline (BB), borderline lepromatous (BL), lepromatous (LL), reversal reaction (R1), and erythema nodosum leprosum (R2). Qualitative and quantitative immunohistochemical analyses were performed to detect CD3, CD4, CD8, FoxP3, CD20, CD138, CD1a, CD57, CD15, CD117, CD68, and CD163. In addition, histochemistry was employed to identify eosinophils. The amount of CD3+ and CD4+ T cells was higher in TT than in LL patients. CD8+ T cells were predominant in T lymphocyte infiltrations in the basal layer of the epidermis. The number of FoxP3+ cells was similar among different forms of the disease, but was higher in BL and LL than in R2 individuals. CD20+ lymphocytes were most abundant in TT samples, while CD138+ plasma cells displayed no detectable differences. Epithelioid macrophages from the center of TT and R1 granulomas exhibited the M1 phenotype (CD68+CD163-), whereas those in LL granulomas showed the M2 phenotype (CD68+CD163+). There was a gradual decrease in the amount of CD1a+ cells from the TT towards the LL form of the disease. A significant increase in the number of neutrophils was observed only in R2 samples. All the cells investigated, except eosinophils, participated in the immunopathogenesis of leprosy.
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