Evaluation of IgM Fc Receptor Expression in Sjögren’s Syndrome

Objectives: Primary Sjögren’s syndrome (pSS) is an autoimmune disease. The causes of pSS are poorly understood and curative treatments are not available. Thus, there is a need to identify causes of pSS in order to improve diagnosis and treatment. Studies show IgG autoantibodies are pathogenic in pSS. However, the role of IgM in disease is poorly understood. The receptor for IgM, termed the Fcμ Receptor (FcμR), is critical in maintaining normal IgM levels and in preventing IgG autoantibody development. Despite its importance, little is known regarding the expression and function of this receptor in pSS. Objective: To determine whether IgM and FcμR levels are altered in B cells from pSS mice.
Methods: We used the pSS mouse model NOD.B10Sn-H2^b/J (NOD.B10) and age and sex-matched C57BL/10 controls. We used flow cytometry to measure IgM and FcμR expression on NOD.B10 B cells derived from the spleen and cervical lymph nodes. We then used quantitative PCR (qPCR) to compared expression of splenic and salivary Fcmr levels. Finally, we sort-purified follicular and marginal zone B cells and used qPCR to assess Fcmr expression.
Results: Our data show the percentage of splenic B cells that express IgM is similar in NOD.B10 mice and controls. In contrast, the percentage of NOD.B10 cervical lymph node B cells that express IgM is decreased in pSS animals. There was no difference in Fcmr gene expression between splenic or salivary tissue derived from NOD.B10 and C57BL/10 females. Finally, NOD.B10 follicular B cells express higher levels of FcmR as compared to the marginal zone subset.
Conclusions: Our preliminary data demonstrate reduced IgM expression in cervical lymph nodes of pSS mice. The FcμR is expressed in NOD.B10 and C57BL/10 splenic and salivary tissue. Further studies are needed to determine whether the FcμR contributes to the loss of B cell tolerance in pSS.