A registry for neonatal lupus established in 1994 provides the authors with a key source of information that permits the translation of clinical information to understanding the underlying science. management of this disease. The Merinoff Symposia is a new entity sponsored by the Feinstein Institute to host scientific meetings focused on important topics in clinical and translational science. The objective is to create dialogue between clinicians and basic science investigators. The major gaps in understanding the nature of SLE and optimal therapeutic approaches indicate the need to provide a venue to assimilate new ideas and key information with the goal of providing an integrated approach to future patient care. Recently, the Feinstein Institute for Medical Research and the Merinoff Foundation cosponsored the first Merinoff Symposium in conjunction with Journal of Internal Medicine. The Symposium entitled Systemic Lupus: Bringing Science to the Patient was held from September 24C27, 2008 in New York. This was a unique platform for discussions of current advances in basic and translational research for this debilitating disease. The environment included clinical investigators, laboratory researchers and trainees, who interacted and talked about basic science models and clinical trials for SLE and the application of this knowledge to patient care. Here we highlight several of the topics discussed at this symposium, as detailed in IPI-493 the following and six reviews [1C6]. These reviews focus on autoimmunity, autoantigens [1], B cell activation [2], T-effector cells [3], autoantibodies in pregnancy [4], cholinergic control of inflammation [5] and genes and genome-wide association studies for SLE [6]. A major challenge to the study of human autoimmune diseases is the heterogeneous and complex nature of multiple potentially interacting parameters encompassing genetic and environmental influences. Rosen and Casciola-Rosen [1] review autoantigens in systemic autoimmunity and discuss the process of antigen selection. The authors propose a model in which neo-antigens are not ubiquitously present but are formed as a result of dynamic interactions that occur between immune effector pathways and specific target tissues. It is these neo-antigens that, in context, then provoke autoreactive immune responses. Rosen [4] present IPI-493 an integrated clinical and research approach for the management of autoimmune associated congenital heart block (CHB), a manifestation of the neonatal lupus syndromes. CHB arises as a result of passively acquired autoimmunity due to antibodies that cross the placental barrier and that react with components of the SSA/RoCSSB/La ribonucleoprotein complex. Eighty-five percent of fetuses identified with CHB are from mothers with antibodies to SSA/RoCSSB/La. This is associated with improved morbidity and mortality to the fetus and neonate. A registry IPI-493 for neonatal lupus founded in 1994 provides the authors with a key source of info that permits the translation of medical info to understanding the underlying technology. The authors discuss their operating model of the pathogenesis, current evaluation strategies, and preventive methods for CHB. Controlled cytokine production occupies a crucial role in keeping homeostasis within the immune system, because unregulated cytokine production mediates inflammation, damage to target organs, and even death. Inflammation is integral to the pathogenesis of autoimmune diseases, and elevated cytokine levels have been implicated in tissue damage in SLE and RA. Rosas-Ballina and Tracey review the cholinergic control of swelling [5] and discuss the concept that inflammation is definitely controlled by neural mechanisms. The cholinergic anti-inflammatory pathway is definitely comprised of the vagus nerve, the neurotransmitter acetylcholine, and the alpha7 subunit of the nicotinic acetylcholine receptor which regulates innate immunity. The authors evaluate the status of this field, and discuss potential restorative applications based on vagus nerve activation and pharmacological activation of this pathway in treating swelling and autoimmunity. A recent flurry of genome-wide association studies (GWAS) have led to reports of several novel SLE risk genes. Graham review the GWAS data for SLE inside a meta-analysis that summarizes 17 validated risk variants for SLE, including four newly confirmed variants [6]. The confirmed SLE risk variants offer an early glimpse into the CSNK1E major pathways dysregulated in human being SLE and include neutrophil function, B cell development and signalling as well as toll-like receptors 7 and 9. The classes included discussions within the induction of autoreactivity having a focus on (i) causes and innate immunity; (ii) adaptive immunity and animal models; two classes on human being disease: (iii) cells reactions and (iv) adaptive immunity; and (v) a final session on genes and gene manifestation. Thirty-eight fascinating presentations were discussed in these classes and.

A registry for neonatal lupus established in 1994 provides the authors with a key source of information that permits the translation of clinical information to understanding the underlying science