I do understand why some medical students cringe at the thought of the lymphatic system. It’s a miraculous albeit complex system where many mysteries of the body take place. For instance, consider this, we have Memory B Cells? Oh yes we do. These cells “are formed from activated B cells that are specific to the antigen encountered during the primary immune response.” Imagine that, while you’re out walking, talking, cheating and lying, your body is forming a little cellular memory miracle separate from your brain.

Years ago when I was diagnosed with hypothyroidism — doctor tried to treat a symptom and not the underlying disease — I was most fascinated with the T’s, T4, T3 and TSH and wondered how endocrinologists keep any of this mess straight. Their heads must explode several times a year.

Learning more about lupus and other autoimmune diseases, I can understand why these diseases are hard to diagnose. There is a party line going on in our bodies and the time needed to research, test, diagnose and treat the underlying cause of our malaise is something our overburdened health care system cannot do. Instead, doctors have to treat symptoms until such time something comes up that gives them a clue.

That leads me to an article I read today at Science Careers on Translating Lupus Research. The article takes us on a journey with Barbara Vilen, an immunologist — bless her heart — and how her encounter with a patient caused her to change scope away from “basic molecular mechanisms and toward work that could be applied to human patients.”

Transitioning from mice to men — and women — Vilen has embarked on a journey into the world of B Cells.

The complexity of lupus makes the disease difficult to study. In lupus patients, so-called self-antigens–nucleic acids and proteins found in every cell’s nucleus–trigger the creation of antibodies that attack otherwise healthy tissue. But that relatively straightforward picture is clouded by the substantial patient-to-patient variations. For example, patients with antibodies to the so-called Smith Antigen, a ribonucleoprotein complex, tend to have more severe disease symptoms than patients without these antibodies. Adding to the difficulty is the fact that the symptoms are intermittent: Patients might present at the clinic one week feeling fine, but the next week have a “flare”–a sudden worsening that can include swollen, painful joints, fever, rashes, and hair loss.

Did your head explode behind reading the above? All kidding aside, Vilen’s work is important because faulty B cells are the central culprit in the disease. Through her research, Vilen discovered that, “in a normal immune system this B cell–regulatory pathway occurred only when the immune response was activated by self-antigens–and not when it was stimulated by bacterial or viral antigens. They had found a new pathway that stopped autoimmunity cold. In lupus patients, Vilen hypothesized, something must have gone wrong with this normal shutdown mechanism.”

Vilen could have stopped there. Instead, she decided to truly go from mice to men and applied for patients. “The idea is to override the malfunctioning signals that allow self-antigens to activate B cells.”

Vilen has teamed up with a rheumatologist and others to further explore autoimmunity transferring what she has learned from mice to humans. She has already learned the stuff of mice does not translate to the stuff of humans. For instance, and here comes those T’s again, “toll-like receptor (TLR) 4, is not very active in human B cells. Instead, human B cells in the lymphoid organs signal mainly through TLR7 and TLR9.”

Okay, now that all of our heads have exploded, the truth is this: to understand autoimmunity, particularly lupus, one must drill down into the body’s cellular structure. Without grants and funding for such research, we won’t fully understand what makes the body tick.  With autoimmune diseases on the rise, time, money and resources are needed to combat the diseases we may see in the future. Let’s face it, starting with my generation, we were the first little babies exposed to processed foods. Now we have tons of the stuff on the market and we now have genetically modified foods.  God only knows what that stuff will do to our cells. It is quite possible what worked in the not-so-good old days — antibiotics, etc. — will not work in the future.

I applaud Ms. Vilen and her team for making the effort and doing the “drill down.” Thank you. I am also glad to know there are still a few people out there who care, as it was in her case when she attended a seminar, to notice “one lupus patient listening intently to each talk”, and that patient stuck with her to the point of shifting gears from mice to men.

“How can you study basic science mechanisms [in humans] when you don’t have enough cells? The only way I can see to do that is to take what we have in the mouse and ask, Does it happen in humans? … If we’re right, we’re golden; if we’re wrong, you get a bad track record. We’re taking a risk. We might be wrong, but at this point we need to at least try.” –Barbara Vilen, UNC