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Epitopes of microbial and human heat shock protein 60 and their recognition in myalgic encephalomyelitis
Amal Elfaitouri1, Björn Herrmann, Agnes Bölin-Wiener
1Section of Clinical Microbiology, Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
Abstract:
Myalgic encephalomyelitis (ME, also called Chronic Fatigue Syndrome), a common disease with chronic fatigability, cognitive dysfunction and myalgia of unknown etiology, often starts with an infection. The chaperonin human heat shock protein 60 (HSP60) occurs in mitochondria and in bacteria, is highly conserved, antigenic and a major autoantigen. The anti-HSP60 humoral (IgG and IgM) immune response was studied in 69 ME patients and 76 blood donors (BD) (the Training set) with recombinant human and E coli HSP60, and 136 30-mer overlapping and targeted peptides from HSP60 of humans, Chlamydia, Mycoplasma and 26 other species in a multiplex suspension array. Peptides from HSP60 helix I had a chaperonin-like activity, but these and other HSP60 peptides also bound IgG and IgM with an ME preference, theoretically indicating a competition between HSP60 function and antibody binding. A HSP60-based panel of 25 antigens was selected. When evaluated with 61 other ME and 399 non-ME samples (331 BD, 20 Multiple Sclerosis and 48 Systemic Lupus Erythematosus patients), a peptide from Chlamydia pneumoniae HSP60 detected IgM in 15 of 61 (24%) of ME, and in 1 of 399 non-ME at a high cutoff (p<0.0001). IgM to specific cross-reactive epitopes of human and microbial HSP60 occurs in a subset of ME, compatible with infection-induced autoimmunity.
Insights
Myalgic encephalomyelitis (ME), or Chronic Fatigue Syndrome, is linked to an immune response against human heat shock protein 60 (HSP60). Specific antibodies (IgM) to HSP60 peptides suggest infection-induced autoimmunity in ME patients.
Area of Science:
- Immunology
- Autoimmunity
- Microbiology
Background:
- Myalgic encephalomyelitis (ME), also known as Chronic Fatigue Syndrome, is characterized by fatigue, cognitive issues, and pain, often triggered by infection.
- Human heat shock protein 60 (HSP60) is a conserved protein found in mitochondria and bacteria, acting as a significant autoantigen.
- The immune response to HSP60, particularly autoantibodies, is implicated in various autoimmune conditions.
Purpose of the Study:
- To investigate the humoral immune response (IgG and IgM) to human and microbial HSP60 in patients with ME.
- To identify specific HSP60 epitopes that elicit an immune response in ME patients, potentially indicating infection-induced autoimmunity.
Main Methods:
- Studied anti-HSP60 IgG and IgM responses using recombinant human and bacterial HSP60, along with 136 peptides from various species' HSP60.
- Employed a multiplex suspension array for high-throughput analysis of antibody binding to HSP60 peptides.
- Validated findings using a selected panel of 25 HSP60-based antigens in a larger cohort of ME and non-ME individuals.
Main Results:
- HSP60 peptides demonstrated binding to IgG and IgM with a preference in ME patients, suggesting a competition between protein function and antibody binding.
- A specific peptide from Chlamydia pneumoniae HSP60 detected IgM in 24% of ME patients, compared to only 1 of 399 non-ME individuals (p<0.0001).
- These findings indicate the presence of IgM to cross-reactive epitopes of human and microbial HSP60 in a subset of ME patients.
Conclusions:
- The study suggests that an autoimmune response targeting HSP60, potentially triggered by microbial infections, occurs in a subset of ME patients.
- The presence of specific IgM antibodies against HSP60 epitopes supports the hypothesis of infection-induced autoimmunity in the etiology of ME.
- Further research into HSP60-related autoimmunity may offer new diagnostic and therapeutic avenues for Myalgic Encephalomyelitis.
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