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Related Experiment Videos

T cells from multiple sclerosis patients recognize multiple epitopes on Self-IgG.

A L K Hestvik¹, F Vartdal, A B Fredriksen

¹Institute of Immunology, Rikshospitalet-Radiumhospitalet Medical Center, University of Oslo, Oslo, Norway.

Scandinavian Journal of Immunology

|September 14, 2007

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Multiple sclerosis patients’ T cells recognize unique IgG idiotope peptides in cerebrospinal fluid. Somatic mutations within these idiotopes are crucial for T-cell recognition, suggesting a role in disease pathology.

Area of Science:

Immunology
Neuroimmunology
Molecular Medicine

Background:

Immunoglobulin (Ig) molecules possess variable regions with immunogenic determinants called idiotopes.
Previous research indicated T cells from multiple sclerosis (MS) patients recognize autologous cerebrospinal fluid (CSF) IgG, with a mapped T-cell epitope on an IgG idiotope.

Purpose of the Study:

To investigate the capacity of CSF IgG molecules to induce a broad polyclonal T-cell response in MS.
To analyze T-cell responses against idiotope peptides within complementarity determining region (CDR) 3 and somatic mutations of monoclonal CSF IgG.

Main Methods:

Analysis of T-cell responses in blood and CSF against idiotope peptides derived from monoclonal CSF IgG.
Peptides spanned CDR3 and included somatic mutations within variable regions.

Related Experiment Videos

T-cell clone recognition assays for idiotope peptides and B-cell clones.

Main Results:

CD4(+) T cells from MS patients recognized multiple idiotope peptides presented by HLA-DR molecules, indicating a diverse idiotope-specific T-cell repertoire.
Somatic mutations were essential for T-cell recognition; mutated CDR1 peptides were recognized, but not corresponding germline peptides.
A specific T-cell clone recognized both an idiotope peptide and the B-cell clone expressing it, suggesting endogenous processing and presentation.

Conclusions:

Mutated CSF IgG in MS patients contains multiple T-cell epitopes.
These epitopes may drive intrathecal IgG production and inflammation in MS via idiotope-driven T-B-cell collaboration.