MONDAY, 24 NOVEMBER 2014
Inflammation is a normal physiological mechanism of the organism in response to harmful stimuli and to initiate a healing process. Inflammation involves a complex and tightly regulated cascade of immunological events. However, persistent tissue injury or an unusual infectious/environmental stimulus can lead to acute or chronic inflammatory diseases.
The researchers discovered that a mutation in the gene Ccdc88b is responsible for the resistance to ECMInterestingly, the human equivalent of Ccdc88b maps to a locus in the human genome that is associated with an increased risk to develop several inflammatory disorders; suggesting relevance of these findings also for humans.
DOI: 10.1084/jem.20140455
Written by Verena Brucklacher-Waldert.
![](mailto:?subject=Inflammation: New regulatory gene identified&body=https://bluesci.co.uk/posts/inflammation-new-regulatory-gene-identified <span style="text-align: justify;">Inflammation is a normal physiological mechanism of the organism in response to harmful stimuli and to initiate a healing process. Inflammation involves a complex and tightly regulated cascade of immunological events. However, persistent tissue injury or an unusual infectious/environmental stimulus can lead to acute or chronic inflammatory diseases.</span><br><br><div class='caption'><div id="attachment_12271" align="alignleft" width="300"><a href="https://bluesci.co.uk/wp-content/uploads/2014/11/148-Image.jpg"><img class="size-medium wp-image-12271" alt="The researchers discovered that a mutation in the gene Ccdc88b is responsible for the resistance to ECM" src="https://bluesci.co.uk/wp-content/uploads/2014/11/148-Image-300x300.jpg" width="300" height="300" /></a> The researchers discovered that a mutation in the gene Ccdc88b is responsible for the resistance to ECM</div></div><span style="text-align: justify;">Researchers from Canada used a chemical mutagen to introduce random mutations into the mouse genome to create a phenotype resistant to Experimental Cerebral Malaria (ECM; a mouse model for neuroinflammation). Subsequently, the researchers screened the entire genome of ECM-susceptible and ECM-resistant mice and discovered that a mutation in the gene <i>Ccdc88b</i> is responsible for the resistance to ECM. Mice carrying this mutated gene show impaired T cell maturation, which is an important feature of inflammatory immune responses. However, the exact mechanism how <i>Ccdc88b</i> affects T cell maturation remains to be elucidated.</span><br><br><span style="text-align: justify;">Interestingly, the human equivalent of <i>Ccdc88b</i> maps to a locus in the human genome that is associated with an increased risk to develop several inflammatory disorders; suggesting relevance of these findings also for humans.</span><br><br><span style="text-align: justify;">DOI: 10.1084/jem.20140455</span><br><br><span style="text-align: justify;">Written by Verena Brucklacher-Waldert.</span>){kind=link}