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Mimicry between HTLV-I and myelin basic protein: no response in HTLV-I-associated myelopathy patients
J M Davies1, S Sonoda, S Yashiki
1School of Biological and Environmental Science, Murdoch University, Western Australia.
Abstract:
The reactivity to a peptide from the HTLV-I polyprotein (FKLPGLNSR) and a similar sequence from myelin basic protein (MBP) (FKLGGRDSR) was examined in relation to the proposal that mimicry of MBP by HTLV-I could be involved in autoimmune responses in HTLV-I-associated myelopathy (HAM). It was found that rabbit antibodies raised against the HTLV-I peptide recognised both peptides, with a titre of 1/10240 to the HTLV-I peptide and 1/5220 to the MBP peptide. Human sera from HAM patients and a HTLV-I carrier without HAM showed slightly higher responses to the HTLV-I peptide compared to the responses from uninfected human sera. HAM patients had greater responses to the HTLV-I peptide than to the similar MBP peptide and an unrelated bovine MBP peptide. There was no recognition of the peptides by peripheral blood lymphocytes from HAM patients or a HTLV-I carrier without HAM. It was concluded that although cross-reactivity was demonstrated in rabbits and the HTLV-I peptide was recognised by sera from HAM patients, the epitope does not appear to evoke a mimicking response to the similar region in MBP. Hence it is not likely to be involved in the pathogenesis of HAM through molecular mimicry.
Insights
Molecular mimicry between human T-lymphotropic virus type I (HTLV-I) and myelin basic protein (MBP) is unlikely to cause HTLV-I-associated myelopathy (HAM). While cross-reactivity was observed, it does not support a significant role in HAM pathogenesis.
Area of Science:
- Immunology
- Neurovirology
- Autoimmune Diseases
Background:
- Human T-lymphotropic virus type I (HTLV-I) infection is linked to HTLV-I-associated myelopathy (HAM).
- A hypothesis suggests molecular mimicry between HTLV-I and myelin basic protein (MBP) may trigger autoimmune responses in HAM.
- Investigating this cross-reactivity is crucial for understanding HAM pathogenesis.
Purpose of the Study:
- To examine the immune response to an HTLV-I peptide and a similar myelin basic protein (MBP) peptide.
- To determine if molecular mimicry between HTLV-I and MBP contributes to autoimmune responses in HAM patients.
Main Methods:
- Antibody reactivity was tested using rabbit antibodies raised against an HTLV-I peptide and human sera from HAM patients, HTLV-I carriers, and uninfected individuals.
- Reactivity to the HTLV-I peptide, a similar MBP peptide, and an unrelated bovine MBP peptide was assessed.
- Peripheral blood lymphocytes from HAM patients and HTLV-I carriers were tested for peptide recognition.
Main Results:
- Rabbit antibodies recognized both HTLV-I and MBP peptides, indicating cross-reactivity.
- Human sera from HAM patients showed higher responses to the HTLV-I peptide than to MBP peptides.
- No significant recognition of the peptides by peripheral blood lymphocytes from HAM patients or HTLV-I carriers was observed.
Conclusions:
- Cross-reactivity between HTLV-I and MBP peptides occurs in rabbits and is detected in HAM patient sera.
- The observed cross-reactivity does not support a significant role for molecular mimicry in the pathogenesis of HAM.
- The HTLV-I epitope studied is unlikely to trigger an autoimmune response to MBP via molecular mimicry in HAM.