ArticleActa neuropathologica2015
M. leprae components induce nerve damage by complement activation: identification of lipoarabinomannan as the dominant complement activator.
Article in Acta neuropathologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Understanding Autoimmune Response Mechanisms in Leprosy.Indian dermatology online journal · 2025Article
- What happens when Schwann cells are exposed toIBRO neuroscience reports · 2023Review
- The systemic inhibition of the terminal complement system reduces neuroinflammation but does not improve motor function in mouse models of CMT1A with overexpressedCurrent research in neurobiology · 2023Article
- Development, Characterization, and in vivo Validation of a Humanized C6 Monoclonal Antibody that Inhibits the Membrane Attack Complex.Journal of innate immunity · 2023Article
- Case report: Injected corticosteroids for treating leprosy isolated neuritis.Frontiers in medicine · 2023Article
- Pathogenicity and virulence ofVirulence · 2022Review
- Gene Expression Profile ofFrontiers in medicine · 2022Article
- Article
- In search of biomarkers for leprosy by unraveling the host immune response to Mycobacterium leprae.Immunological reviews · 2021Review
- The Role of Complement System and the Immune Response to Tuberculosis Infection.Medicina (Kaunas, Lithuania) · 2021Review
- The immunology of other mycobacteria: M. ulcerans, M. leprae.Seminars in immunopathology · 2020Review
- Murine experimental leprosy: Evaluation of immune response by analysis of peritoneal lavage cells and footpad histopathology.International journal of experimental pathology · 2019Article
- Differential Expression of IFN-Journal of immunology research · 2019Article
- Mannose-capped lipoarabinomannan in Mycobacterium tuberculosis pathogenesis.Pathogens and disease · 2018Review
- Systemic inhibition of the membrane attack complex impedes neuroinflammation in chronic relapsing experimental autoimmune encephalomyelitis.Acta neuropathologica communications · 2018Article
- Blood coagulation abnormalities in multibacillary leprosy patients.PLoS neglected tropical diseases · 2018Article
- World leprosy day 2018: How forward respecting the past?The Indian journal of medical research · 2018Article
- Anti-Lipoarabinomannan-Specific Salivary IgA as Prognostic Marker for Leprosy Reactions in Patients and Cellular Immunity in Contacts.Frontiers in immunology · 2018Article
- Innate Immune Responses in Leprosy.Frontiers in immunology · 2018Review
- In Situ complement activation and T-cell immunity in leprosy spectrum: An immunohistological study on leprosy lesional skin.PloS one · 2017Article
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peripheral nerve damage is the hallmark of leprosy pathology but its etiology is unclear. We previously identified the membrane attack complex (MAC) of the complement system as a key determinant of post-traumatic nerve damage and demonstrated that its inhibition is neuroprotective. Here, we determined the contribution of the MAC to nerve damage caused by Mycobacterium leprae and its components in mouse. Furthermore, we studied the association between MAC and the key M. leprae component lipoarabinomannan (LAM) in nerve biopsies of leprosy patients. Intraneural injections of M. leprae sonicate induced MAC deposition and pathological changes in the mouse nerve, whereas MAC inhibition preserved myelin and axons. Complement activation occurred mainly via the lectin pathway and the principal activator was LAM. In leprosy nerves, the extent of LAM and MAC immunoreactivity was robust and significantly higher in multibacillary compared to paucibacillary donors (p = 0.01 and p = 0.001, respectively), with a highly significant association between LAM and MAC in the diseased samples (r = 0.9601, p = 0.0001). Further, MAC co-localized with LAM on axons, pointing to a role for this M. leprae antigen in complement activation and nerve damage in leprosy. Our findings demonstrate that MAC contributes to nerve damage in a model of M. leprae-induced nerve injury and its inhibition is neuroprotective. In addition, our data identified LAM as the key pathogen associated molecule that activates complement and causes nerve damage. Taken together our data imply an important role of complement in nerve damage in leprosy and may inform the development of novel therapeutics for patients.
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