Sjogren's Syndrome and B-cells

B-lymphocyte found here. Could this be the villain?  

I received a link from PubMed the other day leading me to an abstract of a study, which I found very intriguing. The complete study results have yet to be published, this is an Epub ahead of print. I'm looking forward to reading the study in it's entirety.

What caught my attention was the focus on B-lymphocytes in relation to Sjogren's syndrome disease activity.

Why?

Here's an extremely simplified answer to an extremely complex immune response: Current scientific thinking around Ss mechanism is based on the fact that, when studied under a microscope, moisture producing glands and cells are destroyed or altered in Sjogren's syndrome by infiltration of a subtype of a white blood cell: T-lymphocytes. So therapies were investigated which altered T cell activity in the hopes of stopping or diminishing T-lymphocytes' role in the cytokine/inflammatory cycle.

And. Those of us that have been around the autoimmune block a time or two know first hand that there has been very limited success in developing these therapies.

Recent studies, read this and this, indicate that although the current understanding of the T-lymphocyte's role in inflammation and cytokine cell destruction is accurate, there is ANOTHER specialized white blood cell which also may play an active role in this chain of autoimmunity: the B-lymphocyte.

Here's what researchers are hoping: that by inhibiting the B-lymphocyte, the self-destructive chain of events that lead to autoimmunity can be interrupted.

Study abstract found on PubMed, here:

B-cell populations and sub-populations in Sjögren's syndrome. AuthorsHamza N, et al. Journal Presse Med. 2012 Jul 26. [Epub ahead of print] Affiliation: University of Groningen, University Medical Center Groningen, Department of Rheumatology and Clinical Immunology, 9700 RB Groningen, The Netherlands.

"Sjögren's Syndrome (SS) is a chronic inflammatory disorder affecting exocrine glands, in particular the lacrimal and salivary glands. The disease can be primary (pSS) or secondary to other systemic autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus and others. The systemic autoimmune character of pSS is also apparent from the occurrence of (non-organ specific) autoantibodies in this disease. Histopathologically, glandular involvement is characterized by focal accumulation of lymphocytes, particularly around epithelial ducts, with, sometimes, germinal center-like structures. The infiltrates largely consist of T-cells, with a preponderance of CD4-positive T-cells. As a result, the pathology in SS was primarily attributed to T cells. However, a break with the fixation on the role of T cells in pSS came when therapeutic B-cell depletion strategies proved remarkably efficacious in this disease, thereby indicating a major role for B-cells in the immunopathogenesis of pSS. In this regard, a closer look at the composition of B-cells and B-cell sub-populations, both in the peripheral blood and in target tissues, is worthwhile. In this review, we discuss current data on B-cells in pSS. B-cell depletion offers a unique possibility to study the recurrence of (pathogenic) B-cells and their characteristics in pSS patients treated with rituximab. Data on B-cell sub-populations in the peripheral blood and B-cell repertoire in the target tissues following rituximab treatment are discussed as well. We also address their state of activation, repertoire, and relation to B-cell activating factor (BAFF)." (Bolding mine.)

Rituximab, also known as Rituxan. Sound familiar? Yes, this is indeed the drug that I refer to as "mousy". Since my initial infusion cycle last spring, I have noticed increased energy reserves, increased saliva production, and complete absence of the lesions from my subacute cutaneous lupus erythematosus.

Guys. This could be big. Stay tuned.