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IRCM scientists find a novel research model for the study of auto-immune diseases
Date:7/3/2013

tibodies with increasingly stronger bonds to antigens during an immune response.

"Since eliminating AID would in turn completely eliminate affinity maturation and class switching, we focused on an enzyme called UNG, which is also involved in both processes," adds Astrid Zahn, research associate in Dr. Di Noia's laboratory and first author of the study. "When we analyzed mice lacking the UNG gene, we found that affinity maturation was normal but class switching was strongly reduced during acute immune responses, such as the response to immunization and against a viral infection."

"While over 100 AID-deficient patients have been identified, it is striking that only a handful of patients are known to be UNG-deficient," explains Dr. Zahn. "Our study, which shows that chronic antibody responses (those to environmental antigens) remain nearly normal without UNG, can explain why most UNG-deficient individuals are not detected among immunodeficient patients. Nevertheless, because we also found that acute antibody responses were significantly affected, we suspect that UNG-deficient people will, for example, respond very poorly to vaccination. In addition, as this work was conducted as part of a larger ongoing investigation of the complex relationship between AID and UNG, we believe that UNG might possibly act as a tumour-suppressor in B-cell lymphomas."

"Until now, it was difficult to study the relative importance of class switching and affinity maturation, and the impact of these two mechanisms on immune responses," concludes Dr. Di Noia. "Our study provides a novel model to study the contribution of these mechanisms in certain auto-immune diseases such as lupus and rheumatoid arthritis, or some infections like influenza."


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Contact: Julie Langelier
julie.langelier@ircm.qc.ca
514-987-5555
Institut de recherches cliniques de Montreal
Source:Eurekalert

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