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Pregnancy Timeline by SemestersFemale Reproductive SystemFertilizationThe Appearance of SomitesFirst TrimesterSecond TrimesterThird TrimesterFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterDevelopmental Timeline
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October 2, 2012--------News Archive Return to: News Alerts


How to shut down the human immune system response to danger
is just as important as knowing how to initiate an inflammatory response.

WHO Child Growth Charts

       

Researchers Discover Key Mechanism Controlling Inflammatory Response

The molecule, known as p110delta, fine-tunes inflammation to avoid excessive reactions that can damage an organism

Researchers at Queen Mary, University of London have discovered how a key molecule controls the body's inflammatory responses. Their findings are published in Nature Immunology.


A healthy immune system reacts to danger signals,
from microorganisms such as bacteria and viruses,
or from the body's own rogue cells, such as cancer cells.

This tightly controlled reaction starts with an
inflammatory phase that alerts and activates the body
to react against the danger signals.

Once the danger has been cleared,
it is critical that the body's inflammatory phase
is shut down to avoid overreaction.


Control over the timing of inflammation is essential and is disrupted in a range of diseases: inflammation that is triggered too quickly or not controlled appropriately can lead to a potentially lethal endotoxic (septic) shock or, in a more chronic state, contribute to the development of diseases such as cancer, arthritis, asthma and multiple sclerosis.

A better understanding of the control mechanisms involved in orchestrating the body's inflammatory response will help in the development of better and more targeted treatments for a variety of diseases.

Professor Bart Vanhaesebroeck, from the Barts Cancer Institute at Queen Mary, University of London, who supervised the research, said: "For years scientists have been puzzled by the way in which p110delta can both fuel and restrain inflammatory reactions in the body. Thanks to the improved understanding that we have achieved through use of genetics and pharmacology, we have now identified one of the specific pathways that p110delta controls."


Researchers found that p110delta balances
the immune response by regulating a particular
type of immune cell, the dendritic cell.

Dendritic cells sense and initiate an immune response,
primarily provoking inflammation when they
encounter "foreign bodies," including bacteria.

By using dendritic cells from mice that lack
active p110delta, researchers found p110delta controls
the transition of a bacteria-sensing receptor (TLR4)
from the surface of the dendritic cell into its interior,
a key step allowing the dendritic cell
to initiate the shut-down phase of inflammation.


Dr Ezra Aksoy, from the Barts Cancer Institute, the first author of the paper, said: "Temporarily interfering with p110delta activity could allow us to modulate the balance between the inflammatory and anti-inflammatory pathways, opening up new therapeutic avenues to be exploited in the fields of vaccination, cancer immunotherapy and chronic inflammatory diseases."

Original article: http://www.eurekalert.org/pub_releases/2012-09/qmuo-rdk092712.php