In Situ Type 1 Cytokine Gene Expression and Mechanisms Associated with Early Leprosy Progression
Mariane M. A. Stefania b, Celina Maria Turchi Martellib, Thomas Phillip Gillisc d, James L. Krahenbuhld e, the Brazilian Leprosy Study Group
- aTropical Pathology and Public Health Institute, Federal University of Goiás, Goiânia-Go, Goias, Brazil. mstefani@iptsp.ufg.br
- bTropical Pathology and Public Health Institute, Federal University of Goiás, Goiânia-Go, Brazil
- cNational Hansen’s Disease Programs Laboratory at Louisiana State University, Baton Rouge
- dNational Hansen's Disease Programs Laboratory at Louisiana State University, Baton Rouge
- eNational Hansen's Disease Programs Laboratory at Louisiana State University , Baton Rouge
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Abstract
We explored the prognostic value of in situ cytokine patterns in 39 patients with single-skin-lesion paucibacillary leprosy before single-dose therapy, with 3 years of follow-up. Interferon (IFN)-gamma, interleukin (IL)-12, IL-10, IL-4, tumor necrosis factor (TNF)-alpha, and macrophage inflammatory protein (MIP)-1alpha mRNA was quantified in skin biopsy samples at diagnosis, and Mycobacterium leprae DNA was detected in 51.4% of cases. Type 1 immunity predominance with measurable IFN-gamma and undetectable IL-4, which is indicative of effective cell-mediated immunity, is compatible with both the reversal reactions (33.3%) and the resolution of lesions (64.1%) observed. A positive correlation between IL-12 and IFN-gamma indicated type 1 polarization via IL-12. The TNF-alpha/MIP-1alpha correlation implied the TNF-alpha induction of chemokines, which is important for granuloma formation. Positive correlations between key regulatory cytokines-IL-10 and IFN-gamma, IL-10 and IL-12, and IL-10 and TNF-alpha-suggests that there may be some level of an intralesional pro- or anti-inflammatory mechanism essential in avoiding immunopathology.
TL;DRPositive correlations between key regulatory cytokines-IL-10 and IFN-gamma, IL-10and IL-12, and IL- 10 and TNF-alpha-suggests that there may be some level of an intralesional pro- or anti-inflammatory mechanism essential in avoiding immunopathology. (Semantic Scholar)

