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A team of researchers led by Ariel Munitz, Ph.D., of the Department of Clinical Microbiology and Immunology at Tel Aviv University, may have found a new way to limit the progression of colorectal cancer, the second leading cause of cancer-related deaths in the United States and the third most common cancer in men and in women. More than 136,700 people in the U.S. were diagnosed with colorectal cancer in 2009 (the last year for which statistics are available) and 51,848 people in the U.S. died from the disease.

Munitz and his team are focusing their attention on macrophages, large white blood cells that are part of the body's immune system. When a foreign invader such as bacteria enters your blood stream, macrophages secrete certain substances to help kill the bacteria. Sometimes, however, activation of macrophages has damaging effects, including tumor progression. Research has shown that certain immunoglobulin-like receptors-cell surface proteins found on important cells of the immune system-can inhibit macrophage activation. Munitz and his colleagues are studying the effects of a cell-surface molecule called paired immunoglobulin-like receptor B (PIR-B) on macrophage activation in colorectal cancer.

The research is funded by a grant from the Israel Cancer Research Fund (ICRF), a nationwide charitable organization founded in 1975 by a group of American and Canadian researchers, oncologists, and lay people determined to harness Israel's educational and scientific resources in the fight against cancer.  ICRF is the largest U.S.-based charity solely devoted to supporting cancer research in Israel and receives its total income from private donations.

The current ICRF grant has enabled Dr. Munitz and his team to identify that PIR-B suppresses the activities of so-called "tumor-associated macrophages". While ongoing studies in Munitz's group are now focused on understanding how this affects colorectal cancer progression, a team of researchers in Israel and Germany, led by Munitz, has recently shown that PIR-B can limit the devastating effects of idiopathic pulmonary fibrosis (IPF), a progressive lung disease that affects between 132,000-200,000 people in the U.S. Pulmonary fibrosis occurs when lung tissue becomes damaged and scarred, making breathing more difficult.  In most cases, doctors can't pinpoint a cause, thus the condition is termed idiopathic. As the disease worsens people with IPF become progressively more short of breath.  Approximately 50,000 new cases of IPF are diagnosed in the U.S. each year, and as many as 40,000 Americans will die from the disease. Current estimates suggest that the number of individuals diagnosed with IPF is growing and will continue to increase in the U.S. and worldwide.

Lung damage caused by the disease can't be repaired, but medications and therapies, including lung transplantation in selected patients, can sometimes help ease symptoms and improve quality of life.  "IPF is a major cause of morbidity and mortality, with no effective treatment," explained Munitz.  "Therefore, a better understanding of the pathways capable of regulating fibrogenesis is critical for the development of efficacious therapies for this unmet medical need."

Macrophages that reside in the lung, for example, known as alternative activated macrophages (aaMacs) have been shown to play a key role in the development of IPF.  "Surprisingly," said Munitz, "pathways that inhibit macrophage functions, especially in IPF, receive little attention."  The researchers used a mouse model as well as human biopsies taken from patients with IPF to demonstrate that PIR-B can inhibit macrophages known to be active in IPF.