Archive for the ‘Autoimmune Diseases’ category

Replacing IVIG

January 29, 2007

immunoglobin g care of NLMIVIG, intravenous immune globulin, is the intravenous injection of immunoglobulin G taken from more than a thousand plasma donors. For patients recieving this expensive, risky and time-consuming therapy for autoimmune diseases or chronic inflammatory diseases, there may be an alternative soon.

A small part of the current IVIG solution is responsible for disabling interferon gamma, which researchers identify as a significant source of inflammation. Researchers in New York believe they can seperate out, even synthesize the specific portion of the solution that will block interferon gamma. The result could be quick and easy, less expensive injections with less risk of infection. The timeframe? Possibly more than 3 years. The timeframe would be much longer if the active ingredient of this potential treatment were not already being used on human subjects, but if you are an IVIG patient, 3 years may try your patience nonetheless.


Link 2


Poison and M.S.

January 27, 2007

poisonWhen good systems go bad, it makes for odd bedfellows. Cancer happens when your cells fail to self-regulate their own existence, and one of the ways we attack it is with radiation that hurts us as well as the cancer. In M.S., the immune system is the malfunctioning system, and scientists in Portugal are experimenting with another treatment that’s normally deadly to humans. Normally oxygen is good and carbon monoxide is bad. In the twisted world of autoimmune diseases, these roles are reveresed.

The New Scientist today reports that carbon monoxide treatment has shown benefits for M.S. mice. Scientists caused experimental autoimmune encephalomyelitis in the mice, their version of M.S. Next they placed some of the mice in an envoirnment with levels of carbon monoxide that would cause discomfort for humans for 20 days. Those mice breathing the carbon monoxide were considerably less disabled than those breathing normal air.

One of the scientists suggests this can be explained by looking at carbon monoxide’s effects of immune system produced free radicals. In autoimmune diseases like M.S., the immune system may release too many free radicals, and the progression of the symptoms may be affected by their destructive ability. The carbon monoxide indirectly decreases the production of free radicals, and this may be why the M.S. mice fared better than their counterparts.

Cautionary quote:

Pharmaceutical companies are currently working on developing drugs that can deliver carbon monoxide locally within the nervous system, the researchers say. They stress that MS patients should under no circumstances try inhaling carbon monoxide – the gas can be lethal.


Update: M.S. and Parasites

January 19, 2007

parasiteEarlier I reported some confusion as to the explanation given by the South Coast Today regarding the effects of stomach parasites on the course of M.S. in an Argentinian study.

Wednesday’s BBC report on the same subject was more informative. The comparison between the accounts is equally illuminating. When explaining the cause of the results, the BBC explained it thusly:

The scientists said it was possible that the parasites were able to influence the production of T-cells – cells which “dampen down” immune reactions within the body, both ensuring their success, and reducing “autoimmune” illnesses such as MS.

No confusion there. The supposition is that the parasites are suppressing the immune system’s production of immune agents, presumably including both the particular types of T-cells that attack that parasite and those that attack the body’s own myelin surrounding the nervous system. Now read the South Coast Today explanation:

The finding suggests that when the body’s immune system is occupied with an external threat, it might be less likely to misfire, which happens in conditions known as autoimmune disorders.

That explanation posits that any time the immune system is engaged in fighting infection, it doesn’t have the resources to engage in self-destruction. The problem is that the resources the immune system would use to fight a parasitic infection are not the same resources it would use to attack its own myelin. Every T-cell is “keyed”, so that it can only attack a certain type of cell. When it comes into contact with that cell, it divides, increasing the supply of that particular keying of T-cell. If the body’s (insert specific parasite name here) parasite attacking T-cells are busy fighting the parasite infection, it has no effect (that I can think of) on the body’s supply of myelin attacking T-cells.

Only the more general immune suppression ability of parasites that the BBC describes makes sense in explaining the results arrived at. In comparing the accounts, the second lesson we arrive at today is the dependability of sources. The BBC took the time to record a reason that makes sense, even if it is only supposition. The South Coast Today didn’t bother. The latter’s style has the advantage of being ready for the ‘presses’ two days earlier. The former’s style has the advantage of being plausible.

South Coast Today
BBC report

Building a better pancake

January 17, 2007

pancakesWell, better if you have celiac disease. Sufferors of celiac have an autoimmune reaction triggered when they consume gluten, a protein found in wheat and other grains.

Apparently, finding gluten-free foods with similar attributes to the grains we know so well isn’t that easy. The glutens provide much of the texture we’re accustomed to. The Prairie Star reports that researchers (chemists) at the Agricultural Research Service in New Orleans have found a pancake recipe for light and fluffy gluten free pancakes using sweet potatoes and rice.

Apparently the sweet potato ingredients add impressive antioxident content as well. That’s not the sort of thing I think about when I chow on pancakes, but when you have chemists doing the cooking, that is the sort of thing that comes up.

Antibody Therapy for Type I Diabetes

January 14, 2007

Islet cellThe suspect? CD137, a T-cell. The crime? Destroying islet cells. The punishment? An antibody specially tailored to attack CD137. The place? University of Pittsburg (and, uh, the pancreas too depending on your perspective).

In this case, the name of the game is prevention, not a cure. In mice that were predisposed to develop diabetes, the anti-CD137 treatment “significantly” slowed the process, but was not able to completely rid the body of CD137’s impact. The story notes that in taking other T-cells, CD4 and CD25 from the treated mice and placing them in immune-deficient mice with the same predispostion, they were able to prevent onset. I’m still scratching my head over how that last part works. Why would the anti-CD137 treatment have any impact on CD4 and CD25? What happened to the CD137 T-cells in the recipient mice, the ones where onset was prevented? The way the story goes, it explains everything except why the transfer of CD4 and CD25 cells had the preventive impact that it did.

The most valuable part of the study seems to be that it verifies the key role of CD137. Given the scope of the immune system, being able to identify your enemy is a good place to start treatment.


Building a Better Lab Rat

January 14, 2007

 Forbes reports that researchers at the Mayo Clinic have developed an importantA Better Lab Rat research tool in the fight against Rheumatoid Arthritis, a lab rat that mimics the human course of the disease.  These transgenic mice have had a gene associated with R.A. risk in humans spliced into their genome and are showing expected signs of the disease, including the R.A. gender gap.

Obviously it helps to have research subjects that do not have constitutional rights, allowing researchers to study the disease more closely under lab conditions, and test treatments more thoroughly and quickly.

Story: Forbes