Antigen-specific secretion of IFNγ and CXCL10 in whole blood assay detects Mycobacterium leprae infection but does not discriminate asymptomatic infection from symptomatic leprosy.

To advance toward a whole blood assay (WBA)-based test capable of facilitating the diagnosis of paucibacillary (PB) leprosy, we evaluated a prototype in-tube WBA using combinations of Mycobacterium leprae antigens. Blood was collected from newly diagnosed untreated PB (n=38), multibacillary (MB) (n=30), healthy household contacts (HHC) of MB (n=27), and endemic controls (n=61) residing in Goiânia and Fortaleza, Brazil. Blood was incubated with M.

Application of Mycobacterium Leprae-specific cellular and serological tests for the differential diagnosis of leprosy from confounding dermatoses.

Mycobacterium leprae-specific serological and cell-mediated-immunity/CMI test were evaluated for the differential diagnosis of multibacillary/MB, and paucibacillary/PB leprosy from other dermatoses. Whole-blood assay/WBA/IFNγ stimulated with LID-1 antigen and ELISA tests for IgG to LID-1 and IgM to PGL-I were performed. WBA/LID-1/IFNγ production was observed in 72% PB, 11% MB leprosy, 38% dermatoses, 40% healthy endemic controls/EC.

Alterations to antigen-specific immune responses before and after multidrug therapy of leprosy.

This study evaluated the impact of leprosy multidrug therapy (MDT) on cell-mediated immunity (CMI) and antibody responses at diagnosis in untreated paucibacillary (PB) (n=15) and multibacillary (MB) patients (n=15) using a panel of Mycobacterium leprae recombinant antigens (rMLs) (CMI: 46f, ML0276, ML2055, leprosy IDRI diagnostic 1 [LID-1], and ML2629, as negative control; serology: LID-1, 46f, 92f, and 33f, as negative control, and phenolic glycolipid I [PGL-I]) and at 2 time points after MDT (PB: 8-20months; MB: 4-22months). At diagnosis, PB patients produced interferon gamma (IFNγ), and MB patients exhibited low/absent response. Shortly after MDT, IFNγ production in PB patients declined except for LID-1; MB patients produced IFNγ to LID-1.