Autoimmune Suppresant Medications

Two of my friends have Crohns, an autoimmune disorder of the digestive system, and they have both asked me why T1 diabetics don't take immunosuppressants meds like they do. I've never seen anything written about this and did not know how to answer. I guessed that it was because we have insulin and the effects of it must be less harsh than taking immunosuppressant meds. One of them named some new meds she's been taking and told me they were way less harsh than what's she's taken in the past. Anyway, the question seems perfectly resonable, since at the least, these meds would probably extend the pancreas' ability to produce insulin, and I have no idea what the answer is, but I bet someone does. Thanks, Cindy

In Type 1’s, the immune system has already killed off all the existing beta cells (the insulin producing cells in the pancreas), and unfortunately, our bodies don’t grow new beta cells. If we could get on the immunosupressive drugs BEFORE our immune system has killed all our beta cells, then it might do some good. I know that there have been clinical trials of immunosuppressive drugs in newly diagnosed, but I think they’re still ongoing. These drugs are harsh. This is important though because a lot of diabetes research right now is focused on stem cell therapies to grow new beta cells. It’s pretty likely that our immune systems will just kill those new cells off, too, unless we take immunosupressive drugs.


If it were only that simple. The immune suppressive and antiinflammatory drugs which do have some effectiveness against conditions such as MS, lupus or psoriasis, are effective against inflammatory tissue damage, but have not been found to be much help against autoimmune t1. Good idea tho.

Actually there has been some success with immunomodulators and recently diagnosed T1’s/T2s…
(I.E, Remicaide and similar drugs) but so far its just lengthened the honeymoon, not cure the underlying disease.
There has been research in this dept…

Its all about Risk /Benefit.
Even if it were true (of the benefits).
the risk (infections etc) would probably outweigh the benefits

This is not entirely true. If I’m not mistaken, in 2005, UCLA’s Dr. Peter Butler (and colleagues from the Mayo Clinic) showed Evidence of Sustained Islet Turnover even in longstanding type 1 diabetes patients (or it may have been in 2004), which was subsequently validated by researchers at the Joslin Clinic the following year (in 2006).

See Abstract Number 278-OR: “Positivity of C-peptide, GADA and IA2 antibodies in Type 1 Diabetic…”.

Both of these studies prove that longstanding patients with type 1 diabetes continue to generate new islets, but that the immune system destroys new islets as soon as they are generated. The prevailing philosophy was that immunosuppressants are more damaging than insulin replacement (although many patients with hypoglycemia unawareness might disagree), but I would dare say that what is really needed is immunomodulatory agents, and there are 2 or 3 of those now undergoing Phase II or Phase III human clinical trials (notably, otelixizumab and teplizumab now undergoing trials for newly diagnosed patients but could ultimately be expanded to longstanding patients once approved, and there are several other treatments including lisofylline (LSF) also being pursued, although this is not as far along on the development timeframe) and even Diamyd’s vaccine is seen as having the same potential, which has completed Phase II clinical trials for a slightly different purpose, but could theoretically be expanded to longstanding type 1 patients. We could see some interesting treatments in the next 5-7 years, not necessarily without adverse effects, but these could nevertheless change the treatment paradigm for type 1 diabetes.

Here’s an article about parasitic worms, if anyone’s interested.

Thank you for the correction, Scott. I obviously should do more research before I chime in with misinformation! I had no idea T1’s generate new islets… interesting…

Oh ookie - but fascinating. If it would eliminate Clara’s D, I’d say, “Eat the worms, kid.”

It’s my understanding, as well, that a newly diagnosed D still has functioning insulin-producing cells (I guess that would explain the honeymoon phase) and that they do continue to be produced throughout the PWD’s life; they’re just destroyed.

Actually Tolerx (is one) company that is developing a monoclonal antibody for T1’s. There are many others undergoing investigation. They are not “immune suppressants” per se, but instead target the T-cells (CD3 in T1) that are responsible for the attack. They have not (so far) resulted in insulin independence, but do offer some relief from the amount of insulin required. Here is a link to their clinical trial enrollment info:

Note the exclusion criteria - you can’t participate if you’ve had any prior malignancies. In other words, there is probably an increased risk in developing malignancy.

This is true for many Monoclonal Ab’s (I work in the industry), so we have to be careful with these things.


I’d eat the worms, too! Bring 'em on.