An update on Behçet''s disease

Behçet's disease (Adamantiades‐Behçet's disease, ABD) is a multisystemic inflammatory disease, the pathogenesis of which is still a mystery. Many questions are still to be answered and the available diverse data need to be brought together to be compared and analysed. There is at least consensus on the effect of possible, but currently unknown, environmental triggering factor(s) against a background of genetic susceptibility. The possible aetiological factors form a broad spectrum, with infectious agents being the most probable ones. Whatever the stimulus is, the target tissue seems to be the small blood vessels, with various consequences of either vasculitis and/or thrombosis in many organ systems. The endothelium seems to be the primary target in this disease; however, it may just be the subject of the bizarre behaviour of the immune system. The diverse existing data could be interpreted in favour of either explanation. A similar confusion exists about the thrombotic tendency in Adamantiades‐Behçet's disease, in terms of whether a primary hypercoagulability is present or whether it is secondary to inflammation. Recent interesting immunological data promise a way out of the existing dilemma. These findings will be outlined within the context of possible hypotheses and attention will be paid to further investigations that are needed.     

Welcome to the neighborhood: epithelial cell-derived cytokines license innate and adaptive immune responses at mucosal sites

Summary: There is compelling evidence that epithelial cells (ECs) at mucosal surfaces, beyond their role in creating a physical barrier, are integral components of innate and adaptive immunity. The capacity of these cells to license the functions of specific immune cell populations in the airway and gastrointestinal tract offers the prospect of novel therapeutic strategies to target multiple inflammatory diseases in which barrier immunity is dysregulated. In this review, we discuss the critical functions of EC-derived thymic stromal lymphopoietin (TSLP), interleukin-25 (IL-25), and IL-33 in the development and regulation of T-helper 2 (Th2) cytokine-dependent immune responses. We first highlight recent data that have provided new insights into the factors that control expression of this triad of cytokines and their receptors. In addition, we review their proinflammatory and immunoregulatory functions in models of mucosal infection and inflammation. Lastly, we discuss new findings indicating that despite their diverse structural features and differential expression of their receptors, TSLP, IL-25, and IL-33 cross-regulate one another and share overlapping properties that influence Th2 cytokine-dependent responses at mucosal sites.     

Acute injury of the ligaments of the knee: magnetic resonance evaluation

Eleven acutely injured knees and 13 normal knees were examined by magnetic resonance imaging (MRI) to assess the value of this modality in detecting acute ligamentous injury of the knee. The presence of torn ligaments in the injured knees was determined by arthroscopy and/or arthrotomy in ten cases and clinical follow-up in one case. The anterior and posterior cruciate ligaments (ACL and PCL) were demonstrated by sagittal spin echo (SE) images through the intercondylar notch (TE = 30 ms; TR = 2,000 ms). The tibial and fibular collateral ligaments (TCL and FCL) were evaluated on coronal SE images (TE = 30 ms, TR = 200 or 530 ms; TE = 120 ms, TR = 2,000 or 2,120 ms). The ACL and PCL were considered torn on MR if they appeared disrupted or were not seen in their normal anatomical positions. The collateral ligaments were considered torn if abnormal high-intensity signal was noted in adjacent soft tissues on TE = 120 ms images or if disruption of a ligament was apparent. Eleven of 15 torn ligaments and 80 of 81 normal ligaments were correctly identified by these criteria. It is concluded that MR imaging may be useful in detecting acute injury of ligaments of the knee.