Featured Research

from universities, journals, and other organizations

How do white blood cells detect invaders to destroy?

Date:
April 29, 2011
Source:
Cedars-Sinai Medical Center
Summary:
Scientists have discovered how a molecular receptor on the surface of white blood cells identifies when invading fungi have established direct contact with the cell surface and pose an infectious threat.

Scientists at Cedars-Sinai Medical Center have discovered how a molecular receptor on the surface of white blood cells identifies when invading fungi have established direct contact with the cell surface and pose an infectious threat.

The receptor called Dectin-1, studied in the laboratory of David Underhill, PhD, an associate professor in Cedars-Sinai's Inflammatory Bowel and Immunobiology Research Institute, detects fungi and instructs white blood cells whether to expend the energy needed to devour the invading pathogens. The findings are featured as the cover story in the April 28 edition of Nature.

Although scientists long have theorized how immune cells recognize microbial debris sloughed from invading organisms at some distance from themselves, this study establishes a model to explain how immune cells determine when pathogens are directly in contact with their surface and thus pose a significantly greater risk, demanding rapid destruction.

The study is important because it moves scientists one step closer to understanding the mysteries of how our bodies mount an immune response to fight disease.

In early stages of infection, white blood cells patrol the body looking for invading pathogens. Dectin-1, a receptor on the surface of white blood cells, recognizes specific components of fungal cell walls, and alerts or "switches on" the immune cells to prepare to fight the infection.

"Our lab has been studying Dectin-1, which directs white blood cells to eat and kill the fungi that they encounter directly, but to ignore soluble material sloughed off of the fungal surface which does not pose an immediate threat," said Helen Goodridge, PhD, first author on the study and a researcher in the laboratory headed by Underhill. "This is important because phagocytosis and anti-microbial defense responses are energy-intensive and destructive, and should only be used when absolutely necessary."

During phagocytosis, a white blood cell encounters a microbe, engulfs it, and eats it. Once inside the cell, the microbe can be killed using a combination of degradative enzymes, highly reactive chemicals, and an acidic environment.

A molecular structure that the Underhill lab calls a "phagocytic synapse" forms at the surface of the white blood cell when Dectin-1 detects fungi. As a phagocytic synapse forms, two inhibitory proteins that block transmission of signals inside the white blood cell are pushed aside. This allows Dectin-1 to instruct the cell to respond. The phagocytic synapse does not form when Dectin-1 encounters soluble fungal debris, so the white blood cell does not respond.

"The phagocytic synapse resembles another molecular structure, the 'immunological synapse.' It is critical at later stages of an immune response," said Underhill. "It appears that the phagocytic synapse may be an evolutionary precursor of the immunological synapse."

The study was funded by the National Institutes of Health, the American Heart Association, and the Crohn's and Colitis Foundation of America. Underhill, who also directs the PhD Program in Biomedical Sciences and Translational Medicine at Cedars-Sinai, is the Medical Center's Janis and William Wetsman Family Chair in Inflammatory Bowel Disease Research.


Story Source:

The above story is based on materials provided by Cedars-Sinai Medical Center. Note: Materials may be edited for content and length.


Journal Reference:

  1. Helen S. Goodridge, Christopher N. Reyes, Courtney A. Becker, Tamiko R. Katsumoto, Jun Ma, Andrea J. Wolf, Nandita Bose, Anissa S. H. Chan, Andrew S. Magee, Michael E. Danielson, Arthur Weiss, John P. Vasilakos, David M. Underhill. Activation of the innate immune receptor Dectin-1 upon formation of a ‘phagocytic synapse’. Nature, 2011; 472 (7344): 471 DOI: 10.1038/nature10071

Cite This Page:

Cedars-Sinai Medical Center. "How do white blood cells detect invaders to destroy?." ScienceDaily. ScienceDaily, 29 April 2011. <www.sciencedaily.com/releases/2011/04/110429095229.htm>.
Cedars-Sinai Medical Center. (2011, April 29). How do white blood cells detect invaders to destroy?. ScienceDaily. Retrieved July 22, 2014 from www.sciencedaily.com/releases/2011/04/110429095229.htm
Cedars-Sinai Medical Center. "How do white blood cells detect invaders to destroy?." ScienceDaily. www.sciencedaily.com/releases/2011/04/110429095229.htm (accessed July 22, 2014).

Share This




More Health & Medicine News

Tuesday, July 22, 2014

Featured Research

from universities, journals, and other organizations


Featured Videos

from AP, Reuters, AFP, and other news services

Courts Conflicted Over Healthcare Law

Courts Conflicted Over Healthcare Law

AP (July 22, 2014) Two federal appeals courts issued conflicting rulings Tuesday on the legality of the federally-run healthcare exchange that operates in 36 states. (July 22) Video provided by AP
Powered by NewsLook.com
Why Do People Believe We Only Use 10 Percent Of Our Brains?

Why Do People Believe We Only Use 10 Percent Of Our Brains?

Newsy (July 22, 2014) The new sci-fi thriller "Lucy" is making people question whether we really use all our brainpower. But, as scientists have insisted for years, we do. Video provided by Newsy
Powered by NewsLook.com
Scientists Find New Way To Make Human Platelets

Scientists Find New Way To Make Human Platelets

Newsy (July 22, 2014) Boston scientists have discovered a new way to create fully functioning human platelets using a bioreactor and human stem cells. Video provided by Newsy
Powered by NewsLook.com
Gilead's $1000-a-Pill Drug Could Cure Hep C in HIV-Positive People

Gilead's $1000-a-Pill Drug Could Cure Hep C in HIV-Positive People

TheStreet (July 21, 2014) New research shows Gilead Science's drug Sovaldi helps in curing hepatitis C in those who suffer from HIV. In a medical study, the combination of Gilead's Hep C drug with anti-viral drug Ribavirin cured 76% of HIV-positive patients suffering from the most common hepatitis C strain. Hepatitis C and related complications have been a top cause of death in HIV-positive patients. Typical medication used to treat the disease, including interferon proteins, tended to react badly with HIV drugs. However, Sovaldi's %1,000-a-pill price tag could limit the number of patients able to access the treatment. TheStreet's Keris Lahiff reports from New York. Video provided by TheStreet
Powered by NewsLook.com

Search ScienceDaily

Number of stories in archives: 140,361

Find with keyword(s):
Enter a keyword or phrase to search ScienceDaily for related topics and research stories.

Save/Print:
Share:

Breaking News:
from the past week

In Other News

... from NewsDaily.com

Science News

Health News

Environment News

Technology News



Save/Print:
Share:

Free Subscriptions


Get the latest science news with ScienceDaily's free email newsletters, updated daily and weekly. Or view hourly updated newsfeeds in your RSS reader:

Get Social & Mobile


Keep up to date with the latest news from ScienceDaily via social networks and mobile apps:

Have Feedback?


Tell us what you think of ScienceDaily -- we welcome both positive and negative comments. Have any problems using the site? Questions?
Mobile: iPhone Android Web
Follow: Facebook Twitter Google+
Subscribe: RSS Feeds Email Newsletters
Latest Headlines Health & Medicine Mind & Brain Space & Time Matter & Energy Computers & Math Plants & Animals Earth & Climate Fossils & Ruins