Eli C. Lewis

Differences in signaling pathways by IL-1beta and IL-18.

Alpha1-antitrypsin monotherapy prolongs islet allograft survival in mice.

The histone deacetylase inhibitor ITF2357 reduces production of pro-inflammatory cytokines in vitro and systemic inflammation in vivo.

Involvement of graft-derived interleukin-15 in islet allograft rejection in mice.

Mycobacterium tuberculosis induces interleukin-32 production through a caspase- 1/IL-18/interferon-gamma-dependent mechanism.

Responses of IL-18- and IL-18 receptor-deficient pancreatic islets with convergence of positive and negative signals for the IL-18 receptor.

Cisplatin-induced acute renal failure is associated with an increase in the cytokines interleukin (IL)-1beta, IL-18, IL-6, and neutrophil infiltration in the kidney.

Interleukin-32 induces the differentiation of monocytes into macrophage-like cells.

Anti-inflammatory preconditioning by agonists of adenosine A1 receptor.

alpha1-Antitrypsin monotherapy induces immune tolerance during islet allograft transplantation in mice.

Erythropoietin prevents dialysis fluid-induced apoptosis of mesothelial cells.

Association between renal injury and reduced interleukin-15 and interleukin-15 receptor levels in acute kidney injury.

The unique hypusine modification of eIF5A promotes islet beta cell inflammation and dysfunction in mice.

Elimination of negative feedback control mechanisms along the insulin signaling pathway improves beta-cell function under stress.

Interleukin-1beta may mediate insulin resistance in liver-derived cells in response to adipocyte inflammation.

The oral histone deacetylase inhibitor ITF2357 reduces cytokines and protects islet β cells in vivo and in vitro.

Sustained expression of circulating human alpha-1 antitrypsin reduces inflammation, increases CD4+FoxP3+ Treg cell population and prevents signs of experimental autoimmune encephalomyelitis in mice.

Alpha-1 antitrypsin inhibits caspase-1 and protects from acute myocardial ischemia-reperfusion injury.

α-1-antitrypsin gene delivery reduces inflammation, increases T-regulatory cell population size and prevents islet allograft rejection.

α1-Antitrypsin insufficiency is a possible contributor to preterm premature rupture of membranes.

Alpha-1-antitrypsin monotherapy reduces graft-versus-host disease after experimental allogeneic bone marrow transplantation.