Aligning patient values and code status: Choice of Diction's Effect (CODE) study.

Background: Decisions regarding resuscitation after cardiac arrest are critical from ethical, patient satisfaction, outcome, and healthcare cost standpoints. Physician-reported discussion barriers include topic discomfort, fear of time commitment, and difficulty articulating end-of-life concepts. The influence of language used in these discussions has not been tested.

Opposing Roles of Tyrosine Kinase Receptors Mer and Axl Determine Clinical Outcomes in Experimental Immune-Mediated Nephritis.

Glomerulonephritis is one of the most severe manifestations of systemic lupus erythematosus, with considerable morbidity and mortality. There remains a major unmet need for successful management of lupus nephritis. TAM family receptor tyrosine kinases (Mer and Axl) play an important role in the maintenance of immune homeostasis in the kidney.

Stat1 Regulates Lupus-like Chronic Graft-versus-Host Disease Severity via Interactions with Stat3.

Systemic lupus erythematosus (SLE) is a complex multisystem autoimmune disease, characterized by a spectrum of autoantibodies that target multiple cellular components. Glomerulonephritis is a major cause of morbidity in patients with SLE. Little is known about the pathogenesis of SLE renal damage and compromised renal function.

Influenza infection results in local expansion of memory CD8(+) T cells with antigen non-specific phenotype and function.

Primary viral infections induce activation of CD8(+) T cells responsible for effective resistance. We sought to characterize the nature of the CD8(+) T cell expansion observed after primary viral infection with influenza. Infection of naive mice with different strains of influenza resulted in the rapid expansion of memory CD8(+) T cells exhibiting a unique bystander phenotype with significant up-regulation of natural killer group 2D (NKG2D), but not CD25, on the CD44(high) CD8(+) T cells, suggesting an antigen non-specific phenotype.

The role of innate signals in B cell immunity to influenza virus.

Decades of research on mammalian immunity to influenza virus infection have thoroughly established the important contributions made by both the innate and adaptive responses in containing the infection, and in eliminating the virus and protecting from reinfection, respectively. While rapid non-specific innate response is functionally distinct from, yet elegantly complementary to, the delayed-but-specific adaptive response, an increasing number of studies have provided evidence suggesting signals generated during the early innate response can have a significant impact on the quality of the later adaptive response, particularly in the context of influenza virus infection. From these findings emerged the notion that certain innate signals can act directly on B cells, and that this can even help activate virus specific B cells independent of T cell help, marking a major shift away from the current two-signal paradigm of lymphocyte activation.

B7-1/2 (CD80/CD86) direct signaling to B cells enhances IgG secretion.

B cell responses are regulated by Ag recognition, costimulatory signals provided by interaction with helper T cells, and by innate signals. We recently provided evidence for a link between the effects of innate and costimulatory signals on B cells during influenza virus infection, by demonstrating that most B cells in the regional lymph nodes of the respiratory tract enhance surface expression of the costimulator B7-2 (CD86) within 24-48 h following infection via a type I IFNR-dependent mechanisms, a finding we are confirming here. While the role of B7-1/2 for helper T cell activation is well documented, its role in direct B cell regulation is poorly understood.