in which we do some science stuff

So let’s talk about MS, the immune system, and drugs. I got a bunch of emails about my post regarding my visit to the neuro: some wonderful people told me about their experiences with the medications (thank you!), some caretakers told me what they’d seen, and a lot of people wanted more information. I can give info, but only so much. (I’m a textiles teacher/ editor/ knitwear designer/ yoga teacher/ translator, damnit, not a doctor!) This is going to be super, super informal, because I am not a doctor or medical expert of any kind. (BTW, mandatory disclaimer: I’m still not a doctor or medical expert of any kind. Blogs aren’t substitutes for medical advice. Call your doctor for more information, caveat emptor, etc, etc.)

My goal here is to give a rough, layman’s guide on how the immune system works, how it fails to work in autoimmune disease (specifically, multiple sclerosis) and then give an easy- to- understand explanation as to how this monoclonal antibody treatment works. Trust me, it’s going to be a lot clearer than that sounds. I’ve mapped this out. It’s not the most specific lesson I’ve ever given, but I gave it verbally earlier this week and it seemed to stick.

Bare bones here: the immune system is the body’s defense system against parasite and disease. Immune system malfunction results in inflammation, autoimmune disease, and cancer. It’s got a lot going on, but the major players within the human immune system are the white blood cells: lymphocytes, called B cells and T cells. B cells are generated in the marrow of your bones, and T cells are generated by your thymus. (This is ridiculously basic and also isn’t completely accurate. The beginnings of T cells come from bone marrow, too, and actually mature in the thymus, but we don’t need to get stuck in the weeds like this. They aren’t T cells until they finish cooking in the thymus, and “t for thymus” is also wicked easy to remember.)

B- cells and T- cells each have specific jobs. B- cells work as a sort of patrol force; they’re cruising the body, looking for trouble, interrogating each and every cell they encounter. Any time they bump into anything, just imagine that they’re asking for identification. (I always picture this in a very “Papers, please,” sort of way, complete with Christoph Waltz voice.) In the average body, 99 times out of 100 what those B- cells will encounter will “register” as being integral to the organism, as belonging to the body. Sometimes, though, there will be something foreign; let’s say you have a cold, or the flu. In that case, your B- cells find the intruder, register that their “identification” isn’t valid, and then high- tail it back to the T- cells to rat them out.

The T- cells serve as the enforcement squad; they come in and destroy the foreign bodies (we hope). Here’s where autoimmune disease can occur, of course; in multiple sclerosis, B- cells have falsely identified the body’s myelin cells as foreign. Different medications address this in varying ways. Gilenya, my current disease- modifying medication and one of the newer drugs on the market, works by suppressing the release of B- cells; it’s not a massive suppression, I can still go out in public without a face mask and everything. Simply dampening immune response helps quiet disease activity while still allowing my body to heal and do its thing.

These medications- monoclonal antibody treatments- aren’t new at all, really, just newly applied to MS. I wouldn’t be considering it quite yet if it were just entering the market as a brand new drug; I’m an early adopter for tech, but a little more cautious about what I’ll put inside my body. They’re being (and have been) used in rheumatoid arthritis, Crohn’s disease, multiple myeloma, transplant rejection prevention, leukemia, the list runs on. The one we are talking about today, Ocrevus (ocrelizumab), is a version of Rituxan (rituximab), which has been in use since 1997 for non- Hodgkin’s lymphoma and leukemia. (Rituxan has also been being used off- label for MS patients, with remarkable success, as well for patients with lupus and chronic fatigue.)

Rituxan- the original drug, which Ocrevus is based upon- was in RMS and PPMS clinical trials originally, several years back, but the drug company’s patent was going to run out, so they gave things a new name/ face and reset the testing/ approval process. I don’t know how I feel about that, exactly, so whatever it is exactly that I do feel about this, it can’t be whole heck of a lot. Pissed at the delay, certainly. Drug companies and capitalism are what they’ve ever been, though. We’re here now.

The theory behind Ocrevus/ ocrelizumab is relatively simple; it’s an infusion that a patient takes at least several times, potentially with a course of IV steroids beforehand. The drug targets the CD20 protien, which is attached to the exterior of some mature B- cells, and then it destroys the CD- 20 positive B- cells. I’m not going to get into CD- 20- positive B- cells in depth here, but the theory is that these CD- 20 positive B- cells contribute to myelin degeneration (the hallmark of MS). Early trials show Ocrevus/ ocrelizumab binding to B- cells bearing the CD-20 markers and disregarding both stem cells and plasma cells, which allows immune function to continue. B- cells replenish in the host body and with any luck will have “reset” to no longer identify native myelin and axons as foreign invaders. The last trial showed a stunning NEDA (No Evidence of Disease Activity) rate- something like 89%, give or take? I’m still sort of boggling over that.  Hooray, science!

Okay: lots of words, but on re- read with a few days of cooling- off, this still looks pretty clear & coherent to me, so out into the Great Wild Yonder it goes. Let me know if there’s anything you need/ want clarification on, but again: not a doctor or medical professional, not playing one on the Internet: just reading, listening to docs, and watching talks. I’ve included some references below, if you want to do more reading: some are a bit heavy, most are light.

B-cells & T- cells, further reading

Stephen L. Hauser, M.D., et. al, B- Cell Depletion with Rituximab in Relaping- Remitting Multiple Sclerosis”, The New England Journal of Medicine, 14 February 2008.

Anna Azvolinsky, “B Cells Can Drive Inflammation In MS”,, October 2015. 

Sue Hughes, “First Data From Ocrelizumab Phase 3 Studies in MS”,, 8 October 2015.

Baron, B, et al; “Treatment of multiple sclerosis with anti- CD20 antibodies”, DOI: 10.1016/j.clim.2011.04.005, 2011.

Roche Investor Update, 28 September 2015

Neurology Advisor, “‘No evidence of disease activity’ for patients on Ocrelizumab”, MS-, 22 April 2016. 

“The shameful story of Rituximab in Multiple Sclerosis”,, 27 March 2011.

There’s a ton more out there (feel free to look up the clinical trials, etc, if that’s your thing; I’m trying to cut this short and keep it light), email away if you want, hit me up on FB/ Twitter/ IG if we’re connected there. Like I said: I’m still not decided on this as a course of action, but I’m thrilled that it might be an option soon, and I’m very happy that this is the direction the research is hard- pushing toward. For my PPMS friends, holy cats, this could be an epic game- changer. I have my ears perked for that December FDA decision announcement and I’ll let you know what I hear!

  One thought on “in which we do some science stuff

  1. October 7, 2016 at 8:20 pm

    So ….sounds lovely? And the side affects are……

    • October 21, 2016 at 12:30 pm

      Well, there’s a list as long as my arm, with everything from “headaches” to “sudden death”, frankly. Mostly, they list the usuals: chills, fatigue, nausea, PML, autoimmune crash, etc. That’s the way it goes with any treatment we’re offered, unfortunately. I think, when I’m looking at something like this, I need to decide how MUCH risk I’m willing to take at any given time.

      So, with Gilenya, my current med, I’m running the risk of dying from brain infection (PML), heart block, autoimmune crash, and spontaneous infection due to being immunocompromised— that’s my constant state, but also, the chances of any of those things happening are relatively low (I’m JC- virus- negative so far, so PML shouldn’t happen to me; my cardiologist actually compliments my screens, which is a little surreal but also means I don’t worry about heart block; and I’m careful about my overall immune health.)

      Something like this treatment comes in swinging and could/ likely will knock a body down for a minute, but it’s also used relatively frequently (and has a longer record of use in humans than Gilenya does, which, hey, that’s pretty nice).

      Really, it sort of seems like six of one, a half dozen of another, when it comes to risk- avoidance here: do I take a pill every day, which has some chance of nasty side effects, or a couple infusions every few weeks for a year (and then maybe nothing, ever again?) which might have the same side effects? Out of that bouquet of questionable options, those infusions start looking like the “best- worst” option out there. :p

  2. October 24, 2016 at 1:52 pm


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