Yes, I think molecular mimicry can have many aspects of mechanism. It sounds like you are more familiar with the intricacies than I am.
But I found another very interesting article about T-cells and multiple sclerosis:
This article is very good in my opinion because it goes into great detail about all of the different types of T-cells and their function.
Here is a good summary of what the authors believe about T-cells and MS:
"The importance of T-cells in the pathophysiology of MS is suggested by several
lines of evidence. T-cells are located at the active edge of MS lesions, and the presence
of perivascular infiltrates of T-cells throughout the CNS is a consistent feature
in all stages of the disease (Prineas 1975). Patients with MS have a higher frequency
of activated T-cells in their peripheral blood, specifically a higher percentage of
activated myelin-reactive T-cells (Hafler et al. 1985; Zhang et al. 1994). The strongest
genetic risk allele for the development of MS is in the class II HLA-DR locus, and
recently another risk allele has been identified in the class I HLA locus (Yeo et al.
2007), suggesting that antigen presentation to CD4+ and CD8+ T-cells plays a causal
role in the development of disease. In the EAE model, adoptive transfer of myelinreactive
T-cells into the peripheral blood of a previously healthy animal is sufficient
to transfer disease (Zamvil et al. 1985). Together, these findings have led to the
hypothesis that MS is a T-cell-mediated autoimmune disease.
Advances in our understanding of T-cell physiology have expanded our understanding
of their role in MS pathophysiology. It is becoming increasingly clear that
T-cells are not a monomorphic population differing only in their T-cell receptor
(TCR) specificities, but rather they are a diverse mix of proinflammatory and antiinflammatory
subtypes, whose reciprocal interactions we are just beginning to
understand. In this chapter, we review what is known about the specificity and functional
state of T-cells in MS patients. To understand more fully the physiology of
these cells, we examine the factors that enhance or inhibit T-cell activation and the
effector profiles T-cells assume after they are activated. We explore in detail the
regulatory role certain T-cells play in inhibiting autoimmune and other inflammatory
processes and the functional deficiency of these cells in MS. Finally, we discuss how
T-cells specifically affect, and are affected by, the local environment of the CNS."
And here is what the authors conclude about Tr1 regulatory cells and vitamin D:
"Unlike FoxP3+ Treg, Tr1 lineage fate is not determined in the thymus, but rather
Tr1 cells are induced from naïve cells by activation in the setting of the appropriate
conditioning signals. Several stimuli have been shown to result in the induction of
Tr1 cells in vitro. Activating T-cells with CD3/CD28 crosslinking in the presence
of IL-10 and IFNa, or with the combination of dexamethasone and 1-,25-(OH)2
Vitamin D3, both result in Tr1 induction (Levings et al. 2001; Barrat et al. 2002).
The latter combination has been of interest as low levels of Vitamin D have been
identified as an environmental risk factor for MS (Munger et al. 2004). Tr1 cells
can also be induced by crosslinking CD3 with the alternative costimulatory
receptor CD46 (Kemper et al. 2003). Finally, the combination of IL-27 and TGFb
also induces Tr1 cells, and this combination is thought to be the mechanism
through which FoxP3+ Treg modified dendritic cells induce Tr1 formation
(Awasthi et al. 2007)."
So, I believe from my own experience Vitamin D is definitely helping me with my disease. But of course this is only anecdotal. I would think future Vitamin D research on patients with MS is a promising approach to investigate.