How Aimspro works

A forum to discuss Aimspro (Goat Serum) as a possible therapy for MS
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How Aimspro works

Post by Luke » Sat Dec 18, 2004 3:30 pm

Dear Friends,

I would like to share my opinion about this product.

This is what I think is known:
There are two kinds of MHC (Major Histo compatibility Complex) molecule that each cell type recognizes. Cytotoxic T cells bind to peptides that are held in MHC Class I molecules, which are found on most cells in the body. Helper T cells interact exclusively with peptides that are held in MHC Class II molecules, which are found only on antigen-presenting cells (APCs).

This is the only information released to date about Aimspro:
The exact mechanism of action is not totally understood yet. Aimspro is a biotechnology product using polyclonal antibodies. The exact technique cannot be disclosed due to the need for commercial confidentiality. The worldwide patent for the product says that the goat produces antibodies against the HLA class 2 part of the immune system. It causes a cascade whereby the immune system is able to cope with the antigen. However, we do not know enough about the mechanism to make other comments.

Professor Dalgleish stated: "It's all about new pathways. It [Aimspro] inhibits a powerful inflammatory pathway and activates another pathway of the immune system which is over-active in MS. The product induced in Aimspro treatment inhibts this pathway, but the beneficial effects go far beyond the pathway explanation."

What do we know? 1. Aimspro does not regrow myelin within hours. 2. Therefor, the answer must be in an action potential, or nerve impulse...that is the series of changes in membrane potential which result from stimulation of a membrane to threshold. It is due to changes in the concentration of sodium and potassium on the inside and outside of the membrane. 3. An action potential occurs in 3 phases; depolarization, repolarization and hyperpolarization.
a) to depolarize, the membrane must be stimulated to threshold. Threshold stimulus opens the sodium voltage regulated gates and sodium ion rushes into the cell. The inside of the cell becomes positively charged (+40 mV).
b) repolarization occurs when the voltage regulated potassium gates open a fraction of a second after the sodium gates open. Potassium ion rushes out of the cell and the inside of the cell becomes more negative.
c) so much potassium ion rushes out of the cell that it becomes more negative than normal (-85 mV) or hyperpolarized.
d) the complete action potential takes a period of 3-4 milliseconds.

This is a summary of HLA class 1 and 2:
The ability of the T cell receptor to discriminate between class I and II molecules is so refined that the replacement of a single amino acid at a critical position in the receptor's Va region can change the specificity of the T cell receptor from one HLA class to the other. A thymocyte whose T cell receptor engages a complex of an HLA class I and a peptide generally also engages its CD8 coreceptors and down-regulates the expression of the unengaged CD4 molecules. The reverse happens to a thymocyte whose T cell receptor has engaged a complex of an HLA class II molecule and a peptide: it becomes a CD4+ cell. Restriction of the maturing T cells to the expression of either CD4 or CD8 molecules is accompanied by the specification of a developmental program and thus, ultimately, determination of the function of the cell. Generally, CD4+ T lymphocytes become helper T cells that elicit responses from B cells and macrophages, whereas CD8+ T lymphocytes become cytotoxic T cells capable of eliminating target cells identified by the interaction of the T cell receptor and the HLA–peptide complex.

As progenitor cells enter the thymus and proceed toward the center, dividing and differentiating along the way, they express their T cell receptor genes in such a way that each clone produces a receptor specific for a different ligand. As they enter the thymic cortex, thymocytes are given the opportunity to match their newly formed receptors with the abundant HLA–peptide complexes on cortical epithelial cells. Most of these thymocytes do not find ligands that fit the combining sites of their receptors, and since this means that they receive no signal to justify their further existence, they die "by neglect." Only a minority of thymocytes capable of weakly (i.e., with a low affinity) engaging their receptors with HLA–peptide complexes receive a signal that blocks the pathway to apoptosis (i.e., they undergo positive selection). The interaction is not strong enough to hold the thymocyte to a cortical epithelial cell, and after they have disengaged, the thymocyte moves deeper into the thymus.

At the corticomedullary junction and then in the medulla, thymocytes run into hordes of macrophages and dendritic cells (which together are the antigen-presenting cells) that display large quantities of HLA–peptide ligands. The thymocytes are given a second chance to find a match for their receptors, but the setting in which this new trial takes place has changed. These medullary antigen-presenting cells are not just passive displayers of HLA–peptide complexes; they also express molecules that provide costimulatory signals to the maturing thymocytes.

Medullary antigen-presenting cells not only express costimulatory molecules that differ from those of the cortical epithelial cells but also express different proteases (cathepsins) in their lysosomes by which they process the invariant chain and other proteins. As a consequence of these and other differences, a stronger interaction (i.e., one with a higher affinity) between T cell receptors and HLA–peptide ligands becomes possible, and when it takes place, it generates a signal instructing the thymocytes to undergo apoptosis. In this manner, the population of medullary thymocytes is purged of most self-reactive cells that might otherwise initiate an autoimmune response (i.e., it undergoes negative selection).

Cells that survive both positive and negative selection leave the thymus and enter the periphery as naive T cells. Of all the progenitor cells that enter the thymus and proliferate in it, less than 1 percent mature into T cells. In the periphery, naive T cells are probably kept alive by low-affinity interactions with complexes of HLA molecules and self peptides. During an infection, T cells that bind to complexes of HLA molecules and foreign peptides with high affinity are stimulated to initiate an immune response. Thus, high-affinity interactions between T cell receptors of immature cells in the thymus lead to apoptosis, whereas in the periphery they result in cellular proliferation. The mechanisms responsible for this difference in behavior remain unidentified.

Once a few hundred of the more than 10,000 receptors displayed by a single T cell become engaged by a ligand, the T cell is activated to differentiate either into a CD8+ cytotoxic killer T cell (if the engaging HLA molecule is of the class I type) or into a CD4+ helper T cell (if the engagement involves a class II molecule). The activities of the stimulated helper T cell include the production of interferon-7, along with other cytokines.

Interferon-7 binds to the regulatory regions of selected genes, including the class II genes and loci that control specialized subunits of proteasomes. The binding enhances the expression of these genes, increasing the number of class II molecules on antigen-presenting cells and altering the composition of the subunits of proteasomes. These modified "immunoproteasomes" are more effective than housekeeping proteasomes at generating peptides for loading onto the class I molecules. Both processes enhance the ongoing immune response.

For continued results, Aimspro must change CD8+ cytotoxic T cells into type CD4+ helper T cells. Hence: "The goat produces antibodies against the HLA class 2 part of the immune system. It causes a cascade whereby the immune system is able to cope with the antigen."

Best regards.


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Post by bromley » Sun Dec 19, 2004 7:39 am


Aimspro results are, I understand, due in mid 2005 - I think the trial only included those with SP ms.

Your post is titled 'how aimspro works' - have you any feel / knowledge that it does work? To date we have only heard anectdotal evidence of people walking again / walking further etc.

Your post is way above my head - but the sense I get is that you feel that this treatment has a different mechanism to other treatments on the market.

Thanks for the information


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Post by Luke » Sun Dec 19, 2004 8:54 am


You're right. Actually, I have no evidence that Aimspro works.

I should have entered subject "If Aimspro works - Here's my theory."

Take care.


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Post by RicMa » Sun Dec 19, 2004 3:00 pm

If I am not wrong, a trial involving Aimspro in ON has just been completed.

Results should come out in the close future.

I hope for a positive outcome, Aimspro looks very promising and is one of the very few drugs targeting (also) progressive MS.


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