Minocycline and EPA are used to treat auto immune conditions and HD. In HD the immune system is activated. Folks with excessive CAG (Q) counts have immunity against many cancers. It is tempting to think that HD is an auto immune condition caused by the extra Qs.

MS and Lyme disease are considered in the diagnosis of HD without a known family history. In the following abstract the researchers suggest these two central nervous system (CNS) diseases may be caused by molecular mimicry. In my opinion this work also suggests that the ever expanding Qs trigger the heightened immune response and the untreated devastation of HD. A researcher might say that the basic principles of cross-recognition and their pathogenetic significance could be relevant in HD --Jerry 17-May-2001
From: J Autoimmun 2001 May;16(3):187-92, Martin R, et al.

Molecular Mimicry And Antigen-specific T Cell Responses In Multiple Sclerosis And Chronic CNS Lyme Disease.

The concept of molecular mimicry provides and elegant framework as to how cross-reactivity between antigens from a foreign agent with self proteins may trigger autoimmune diseases.

While it was previously thought that sequence and structural homology between foreign and self proteins or the sharing of T cell receptor (TCR) and MHC(Major Histocompatibility(immune tolerance) Complex) -binding motifs are required for molecular mimicry to occur, we have shown that even completely unrelated peptide sequences may lead to cross-recognition by T cells.

The use of synthetic combinatorial peptide libraries in the positional scanning format (PS-SCL) together with novel biometric prediction approaches has allowed us to describe the recognition profiles of individual autoreactive T cell clones (TCC) with unprecedented accuracy.

Through studies of myelin-specific TCC as well as clones from the nervous system of patients suffering from chronic central nervous (CNS) Lyme disease it has become clear that at least some T cells are more degenerate than previously anticipated.

These data will not only help us to redefine what constitutes specific T cell recognition, but also allow us to study in more detail the biological role of molecular mimicry. A recent clinical trial with an altered peptide ligand (APL) of one of the candidate myelin basic protein (MBP) epitopes in MS (amino acids 83-99) has shown that such a modified MBP peptide may not only have therapeutic efficacy, but also bears the potential to exacerbate disease.

Thus, we provide firm evidence that the basic principles of cross-recognition and their pathogenetic significance are relevant in MS.