TOL, you're right about Neurovax. There are a few postings that refer to it, and here is a fairly recent example:
I also noticed that estrogen has been found to influence FOXP3
A potential role for estrogen in experimental autoimmune encephalomyelitis and multiple sclerosis.
Ann N Y Acad Sci. 2006 Nov;1089:343-72
Offner H, Polanczyk M.
Neuroimmunology Research, Veterans Affairs Medical Center, 3710 SW U.S. Veterans Hospital Rd., Portland, OR 97239, USA. firstname.lastname@example.org
The extensive literature and the work from our laboratory illustrate the large number of complex processes affected by estrogen that might contribute to the striking ability of 17-beta estradiol (E2) and its derivatives to inhibit clinical and histological signs of experimental autoimmune encephalomyelitis (EAE) in mice. These effects require sustained exposure to relatively low doses of exogenous hormone and offer better protection when initiated prior to induction of EAE. The E2 mediates inhibition of encephalitogenic T cells, inhibition of cell migration into central nervous system tissue, and neuroprotective effects that promote axon and myelin survival. E2 effects on EAE are mediated through Esr-1 (alpha receptor for E2) but not Esr-2 (beta receptor for E2), as are its anti-inflammatory and neuroprotective effects. A novel finding is that E2 upregulated the expression of FoxP3 that contributes to the activity of CD4 + CD25 + T regulatory cells (Treg). The protective effects of E2 in EAE suggest its use as a therapy for multiple sclerosis (MS). Possible risks may be minimized by using sub-pregnancy levels of exogenous E2 that produced synergistic effects when used in combination with another immunoregulatory therapy. Alternatively, one might envision using E2 derivatives alone or in combination therapies in both male and female MS patients.
Last, but not least, some form of t-cell vaccination seemed to help through its influence on FOXP3...
CD4+ regulatory T cell responses induced by T cell vaccination in patients with multiple sclerosis.
Proc Natl Acad Sci U S A. 2006 Mar 28;103(13):5024-9. Epub 2006 Mar 17.
Hong J, Zang YC, Nie H, Zhang JZ.
Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA.
Immunization with irradiated autologous T cells (T cell vaccination) is shown to induce regulatory T cell responses that are poorly understood. In this study, CD4(+) regulatory T cell lines were generated from patients with multiple sclerosis that received immunization with irradiated autologous myelin basic protein-reactive T cells. The resulting CD4(+) regulatory T cell lines had marked inhibition on autologous myelin basic protein-reactive T cells and displayed two distinctive patterns distinguishable by the expression of transcription factor Foxp3 and cytokine profile. The majority of the T cell lines had high Foxp3 expression and secreted both IFN-gamma and IL-10 as compared with the other pattern characteristic of low Foxp3 expression and predominant production of IL-10 but not IFN-gamma. CD4(+) regulatory T cell lines of both patterns expressed CD25 and reacted with activated autologous T cells but not resting T cells, irrespective of antigen specificity of the target T cells. It was evident that they recognized preferentially a synthetic peptide corresponding to residues 61-73 of the IL-2 receptor alpha chain. T cell vaccination correlated with increased Foxp3 expression and T cell reactivity to peptide 61-73...