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A potential role for complement in immune evasion by Mycobacterium leprae
Donato Callegaro-Filho1, Niraj Shrestha, Anne E Burdick
1Department of Microbiology and Immunology, Miller School of Medicine, University of Miami, Miami, FL, USA.
Journal of Drugs in Dermatology : JDD
|November 11, 2010
Summary
Lepromatous leprosy involves immune evasion by Mycobacterium leprae. The bacteria
Area of Science:
- Immunology
- Microbiology
- Infectious Diseases
Background:
- Lepromatous leprosy is characterized by immune evasion, allowing Mycobacterium leprae proliferation.
- The precise mechanism of this immune escape remains largely unknown.
Purpose of the Study:
- To elucidate the mechanism by which Mycobacterium leprae evades the host immune system.
Main Methods:
- Investigated the role of phenolic glycolipid-1 (PGL-1) in M. leprae-infected dendritic cells.
- Examined complement activation and colocalization with PGL-1 in dendritic cell membranes.
- Analyzed the interaction within the immune synapse during T cell co-culture.
Main Results:
- Phenolic glycolipid-1 (PGL-1) from M. leprae is expressed on infected human dendritic cells, activating complement.
- PGL-1 and complement component C3 colocalize in dendritic cell lipid rafts and the immune synapse.
- Activated C3 costimulates naive T cells via CD46, promoting IL-10-secreting regulatory T cell differentiation.
Conclusions:
- Mycobacterium leprae may utilize PGL-1 to subvert host immunity.
- This interaction potentially drives an adaptive immune response that favors bacterial survival.
- A novel immune evasion strategy involving complement activation and regulatory T cell induction is proposed.
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