Year-end Sale % OFF 
Abstract
In leprosy, lepromatous form of the disease is more severe and results from suppression of T cell response. T regulatory cells which suppress T cell response has been found in higher frequency in blood and at the site of infection in leprosy. Therefore, present study was carried out to evaluate the role of Mycobacterium leprae antigens whole cell sonicate (WCS) and especially phenolic glycolipid-1 (PGL-1), which is known for its suppressive nature, in the induction of T regulatory cells expansion in peripheral blood of leprosy patients. For this purpose peripheral blood mononuclear cells (PBMCs) of different category of leprosy patients and healthy controls were stimulated with M. leprae antigens in vitro and percentage of T regulatory cells was determined by flow cytometry. We found higher frequency of T regulatory cells in PBMCs of untreated borderline lepromatous/lepromatous leprosy (BL/LL) patients. Further, PBMCs of untreated BL/LL patients also showed higher percentage of T regs after stimulation with PGL-1. Antigen mediated expansion of T regulatory cells was also supported by results of Carboxy fluorescein succinimidyl ester (CFSE) proliferation assay. None of the antigen induced T regs expansion in healthy controls, untreated tuberculoid/borderline tuberculoid (TT/BT) leprosy patients and treated leprosy patients. Therefore it is suggested that increased frequency of T regs in BL/LL patients may be due to the induction of T regs expansion mediated by PGL-1 of M. leprae and this high percentage of T regs resulted in T cell suppression in lepromatous disease.
Highlights
Leprosy is a chronic infectious disease caused by an intracellular obligate organism Mycobacterium leprae (M. leprae) that affects mainly nerves, skin and mucous membrane
Increased frequency of T regulatory cells in untreated lepromatous leprosy patients To study the difference in T regulatory cells frequency among different category of untreated leprosy patients, completely treated leprosy patients and healthy controls, we studied the frequency of CD3+CD4+CD25+FoxP3+ T regulatory cells by flowcytometry in the blood of these study subjects and percentage was determined using FACS Diva software (Figure 1)
To determine whether the M. leprae antigens induce the expansion T regulatory cells we first isolated peripheral blood mononuclear cells (PBMCs) from the blood of untreated the disease. At tuberculoid (TT)/borderline tuberculoid (BT) and borderline lepromatous (BL)/LL patients, treated tuberculoid/borderline tuberculoid (TT/BT) and borderline lepromatous/lepromatous leprosy (BL/LL) patients and healthy controls and stimulated with whole cell sonicate (WCS) and phenolic glycolipid-1 (PGL-1) for 24 hrs and the frequency of CD3+CD4+CD25+FoxP3+ T regulatory cells was detected by flow cytometry
Summary
Leprosy is a chronic infectious disease caused by an intracellular obligate organism Mycobacterium leprae (M. leprae) that affects mainly nerves, skin and mucous membrane. At tuberculoid (TT) pole patients develop strong delayed type of immune response and limit the growth of the bacteria while lepromatous (LL) pole cellular immune response of the patients selectively fails to respond to the antigens of M. leprae which results in uncontrolled bacterial growth. Between these polar forms borderline tuberculoid (BT), borderline borderline (BB) and borderline lepromatous (BL) forms occur [1,2]. A recently discovered subpopulation of T cells which is CD4+ CD25+ (IL-2 receptor β chain) regulatory T cell expressing Fork head box protein (FoxP3) transcription factor play role in the suppression and regulation of immune response to self and nonself antigens. Their suppressive function needs direct cellcell contact or release of anti-inflammatory cytokines interlukine-10 (IL-10) and transforming growth factor–β (TGF-β) or both [6-
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
