“Seemingly remote studies in basic science of immunology can lead to new therapeutics. That’s the promise of basic research.  But it also takes time, commitment and a lot of resources.” - Carl Ware, Ph.D.

Dr. Ware is Head of the Division of Molecular Immunology at LIAI and adjunct Professor of Biology at UC San Diego . Dr. Ware's research focuses on an important group of cytokines produced by white blood cells called tumor necrosis factors (TNF), which control inflammation and host defenses to pathogens. His laboratory is unraveling the molecular mechanisms of how persistent viruses evade immune defenses providing insight into how the immune response is regulated.

Dr. Ware completed his B.S. in 1974 and his Ph.D. in Molecular Biology and Biochemistry in 1979 at the University of California, Irvine. Dr. Ware began his postdoctoral work at the University of Texas Health Science Center in the Department of Biochemistry, and in 1981 he moved to the Dana-Farber Cancer Institute, Boston, Massachusetts, to complete his postdoctoral training. Dr. Ware returned to California as an Assistant Professor of Immunology at University of California, Riverside in 1982, advancing to full professor in 1992. In 1996, Dr, Ware joined the faculty at LIAI as a full Member and Head of the Division of Molecular Immunology.

Dr. Ware serves on several granting agencies and foundations supporting biomedical research including the Arthritis National Research Foundation, the Sandler Program in Asthma Research and the National Institutes of Health. In addition, he serves as Councilor for the International Cytokine Society and is past president of the International Congress on TNF related Cytokines. Dr. Ware is recipient of a National Merit Award from National Institute for Allergy and Infectious Diseases.

Dr. Carl Ware, Ph.D., and his team study cytokines, proteins that act as communication signals between white blood cells and surrounding tissues. Their goal is to understand the basic molecular and cellular processes of how cytokines regulate immunity to viruses and translate that information into new therapies to control persistent viral infections, autoimmune diseases, and cancer.

The laboratory focuses on cytokines related to tumor necrosis factor (TNF), one of more than 20 related proteins (TNF superfamily) believed to have important roles in the ability of the immune system to guard the body against harmful microbes. Dr. Ware is a leading authority in the field of cytokines, having discovered several members of the TNF superfamily and how these cytokines control inflammation.

When improperly produced, TNF causes painful inflammation associated with diseases such as arthritis. Drugs that block TNF have led to new clinical treatments for arthritis, and TNF inhibitors, such as Enbrel and Remicade, are now FDA-approved for use in rheumatoid arthritis and inflammatory bowel disease. These drugs, known as biologics, are the first generation of therapeutics directed at blocking TNF, but they are not effective in all patients and have serious side effects.

Members of Dr. Ware's laboratory are discovering new ways to modulate TNF-related cytokines that may benefit patients with autoimmune disease. As a result of this research, new biologics, directed to TNF related cytokines are being created that can modulate inflammation and immunity. Interestingly, these same cytokines can be used to induce immunity to pathogens, such as viruses and bacteria, or to cancer. Ongoing work in the laboratory is redirecting these cytokines to applications in infectious and malignant diseases.

A lymphotoxin-IFN-beta axis essential for lymphocyte survival revealed during cytomegalovirus infection. J Immunol, 2005

Cutting edge: a novel viral TNF receptor superfamily member in virulent strains of human cytomegalovirus. J Immunol, 1999

Lymphotoxins and cytomegalovirus cooperatively induce interferon-beta, establishing host-virus detente. Immunity, 2001

Evolutionarily divergent herpesviruses modulate T cell activation by targeting the herpesvirus entry mediator cosignaling pathway. PNAS, 2005

LIGHT expression by mucosal T cells may regulate IFN-gamma expression in the intestine. J Immunol, 2004

LIGHT is constitutively expressed on T and NK cells in the human gut and can be induced by CD2-mediated signaling. J Immunol, 2005

Genomic characterization of LIGHT reveals linkage to an immune response locus on chromosome 19p13.3 and distinct isoforms generated by alternate splicing or proteolysis. J Immunol, 2001

LIGHT-HVEM signaling and the regulation of T cell-mediated immunity. Cytokine Growth Factor Rev, 2003

Turning on LIGHT. J Clin Invest, 2001

Intrinsic lymphotoxin-beta receptor requirement for homeostasis of lymphoid tissue dendritic cells. Immunity, 2005

Human cytomegalovirus UL144 open reading frame: sequence hypervariability in low-passage clinical isolates. J Virol, 1999

LIGHT, a new member of the TNF superfamily, and lymphotoxin alpha are ligands for herpesvirus entry mediator. Immunity, 1998

Lymphotoxin and LIGHT signaling pathways and target genes. Immunol Rev, 2004

B and T lymphocyte attenuator regulates T cell activation through interaction with herpesvirus entry mediator. Nat Immunol, 2005

Constitutive expression of LIGHT on T cells leads to lymphocyte activation, inflammation, and tissue destruction. J Immunol, 2001

Network communications: lymphotoxins, LIGHT, and TNF. Annu Rev Immunol, 2005

The LIGHT and DARC sides of herpesvirus entry mediator. PNAS, 2005

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