Immune Memory Formation Seen In Early Stages Of Viral Infection

In an acute viral infection, most of the white blood cells known as T cells differentiate into cells that fight the virus and die off in the process. But a few of these “effector” T cells survive and become memory T cells, ensuring that the immune system can respond faster and stronger the next time around.

Scientists have identified a molecule that defines which cells are destined to become memory T cells just a few days after a viral infection begins. The finding could guide the development of more effective vaccines for challenging infections such as HIV/AIDS and also cancer.

The results were published online by the journal Immunity. The senior author is Rafi Ahmed, PhD, director of the Emory Vaccine Center, a Georgia Research Alliance Eminent Scholar and a member of the National Academy of Sciences.

Working with Ahmed, postdoctoral fellows Vandalia Kalia and Surojit Sarkar tracked memory T cell formation in mice infected with lymphocytic choriomeningitis virus, a virus that causes an acute infection. They observed that a few days after infection begins, T cells separate into two groups: one with high levels of the molecule CD25 on their surfaces and one with low levels of CD25. Later on, all T cells reduce their levels of CD25 and the differences disappear as the infection is cleared.

“The outstanding question in our field has been: when do T cells commit to becoming memory cells,” Kalia says. “This is one of the earliest points where we have been able to see these groups of cells with distinct fates.” Read more

Cancer/Inflamation Link Discovered By University Of Montreal

Canadian researchers have discovered a novel molecular mechanism that prevents cancer. In the December 11 edition of the prestigious journal Molecular Cell, scientists from the Université de Montréal and the Université de Sherbrooke explain how they found that the SOCS1 molecule prevents the cancer-causing activity of cytokines, hormones that are culprits in cancer-prone chronic inflammation diseases such as Crohns, in smokers and people exposed to asbestos.

“Excessive cytokine activity promotes cancer,” says Dr. Gerardo Ferbeyre, senior author and a Université de Montréal biochemistry professor. “Discovery of these mechanisms will enable scientists to design a cancer-prevention strategy for people with chronic inflammatory diseases and lead to better understanding of the human body’s natural defenses against cancer.”

The research team didn’t anticipate that SOCS1 would turn out to be linked to p53, the master regulator of natural anticancer defenses. “We were surprised to realize that SOCS1 was directly linked to p53,” says first author and Université de Montréal student, Viviane Calabrese.
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Dermatologic Infections In Cancer Patients Treated With EGFRI Therapy

Patients who experience dermatologic toxic effects from epidermal growth factor receptor inhibitors (EGFRIs) have a high prevalence of skin and nail infections, according to a new study published online December 9 in the Journal of the National Cancer Institute.

This new class of anticancer agents, the EGFRIs, is used against various cancers including lung, pancreatic, breast, head and neck, and colorectal cancers. Patients treated with EGFRIs frequently experience toxic effects such as eruptions of the face, dry, itchy skin and nail inflammation. These side effects affect quality of life, but the impact of these effects on the patients’ physical health, such as their increased susceptibility to cutaneous infections, has not been ascertained.

To examine this issue, Mario E. Lacouture, M.D., at the department of dermatology at Northwestern University in Chicago, and colleagues collected data on 221 patients who were treated in a referral clinic for dermatologic toxic effects of EGFRIs. They examined associations between patient characteristics and the development of these infections. Read more

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