Maybe MD2 was right, there is no specific target in the OCB

M

In this study they looked at the specificity of the oligoclonal bands and came to the conclusion that they react to nothing that is consistent. We (the Royal we..i.e. one) have been hunting for years and the same answer has been there in every, yep every study….in that there is no consistent target in the oligolonal bands.

B cells get in the CNS an survive for a very long time.

MD2 came up with an idea that you don’t need to have specific oligoclonal bands. A better idea than most I think.

They are important as they keep the glia activated.

Oligoclonal IgG antibodies in multiple sclerosis target patient-specific peptides. Graner M, Pointon T, Manton S, Green M, Dennison K, Davis M, Braiotta G, Craft J, Edwards T, Polonsky B, Fringuello A, Vollmer T, Yu X.PLoS One. 2020 Feb 21;15(2):e0228883. 

But hey what do I know

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4 comments

  • “In addition, we showed that these peptides represent epitopes sharing sequence homologies with proteins of viral origin,”

    “Although homologous peptides were found within individual patients, no shared peptide sequences were found among any of the 42 MS and 13 inflammatory CSF control specimens”

    So; if ALL ms patients are infected with ebv they would shared some sort of antibody production against Ebv those targets

    Guess this sugests personalized responses rather than a unitfied response against a common target (Ebv)

    • You are making an assumption that molecular mimicray is important for the link between autoimmunity and EBV…it doesn’t have to be

      • The question of shared peptide sequences

        Or non-shared or “private” disease-specific TCRs

        Its also see when you look at the t TCR-β Repertoire in Patients with Neurological Immune-mediated Disorders

        While HAM/TSP patients showed a higher clonal T-cell expansion compared to MS and HCincrease of the TCR clonal expansion was inversely correlated with the diversity of TCR repertoire in all subjects. In addition, longitudinal analysis of TCR repertoires from HAM/TSP patients demonstrated a correlation of the TCR clonal expansion with HTLV-I proviral load. Surprisingly, MS patients showed a higher diversity of TCR repertoires than other groups. Despite higher TCR clonal expansions in HAM/TSP patients, no disease-specific TCRs were shared among patients. Only non-shared or “private” TCR repertoires was observed.

        Comprehensive Analysis of TCR-β Repertoire in Patients with Neurological Immune-mediated Disorders
        https://www.nature.com/articles/s41598-018-36274-7

        It seems logic that when you have an virus causing disease you such have some sort of shared ” ‘signature”

        Both in the b and the t cell compartment

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