Myelodysplastic syndromes (MDS) are a heterogeneous group of hematological malignancies with a high risk of transformation to acute myeloid leukemia (AML). MDS are associated with posttranslational modifications of proteins and variations in the protein expression levels. In this work, we present a novel interactomic diagnostic method based on both protein array and surface plasmon resonance biosensor technology, which enables monitoring of protein-protein interactions in a label-free manner. In contrast to conventional methods based on the detection of individual biomarkers, our presented method relies on measuring interactions between arrays of selected proteins and patient plasma. We apply this method to plasma samples obtained from MDS and AML patients, as well as healthy donors, and demonstrate that even a small protein array comprising six selected proteins allows the method to discriminate among different MDS subtypes and healthy donors.

Sjögren’s disease (SjD) is a heterogeneous autoimmune disease characterized by severe dryness of mucosal surfaces, particularly the mouth and eyes; fatigue; and chronic pain. Chronic inflammation of the salivary and lacrimal glands, auto-antibody formation, and extra-glandular manifestations occur in subsets of patients with SjD. An aberrant expression of long, non-coding RNAs (lncRNAs) has been described in many autoimmune diseases, including SjD. Here, we review the current literature on lncRNAs in SjD and their role in regulating X chromosome inactivation, immune modulatory functions, and their potential as biomarkers.

Salivary gland dysfunction is a hallmark of Sjögren’s disease (SjD). Here, we investigated the pro-inflammatory properties of salivary gland-derived fibroblasts (SGF) that were cultured from minor salivary gland (MSG) tissues of patients with SjD and controls. SGF from patients with SjD exhibited higher rates of proliferation compared to controls. RNA sequencing revealed pronounced pro-inflammatory properties of SGF in response to stimulation with IL1 and polyI:C, with an activation of “interferon responses”, “JAK STAT”, and “NF-kappa B” signaling, as well as ”complement” pathways. In addition to encoding pro-inflammatory transcripts, stimulated SGF featured increased expression of a number of non-coding enhancer RNAs (eRNAs) that we originally identified in TNF-stimulated synovial fibroblasts (FLS) by CAGE sequencing. We confirmed the expression of selected eRNAs in SGF and FLS through time-course experiments upon stimulation with different pro-inflammatory stimuli using real-time PCR. Furthermore, we detected eRNAs for IL6 (eIL6) and IL8 (eIL8#3) in MSG tissues. Treatment of SGF with the bromodomain inhibitor I-BET suppressed IL1- and LPS-induced expression of all eRNAs tested, as well as their associated pro-inflammatory coding transcripts. Transfection of SGF with antisense nucleotides targeting eCCL20 reduced the LPS-induced expression of this eRNA, as well as CCL20 expression and secretion. Together, our data highlight similarities between SGF and FLS regarding their activation under inflammatory conditions.