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ShareJune 28, 2013 — Scientists at an Academy of Finland Centre of Excellence have discovered a new mechanism regulating the immune response that can leave a person susceptible to autoimmune diseases.
A fresh study by Turku Centre for Biotechnology and Aalto University in Finland is the first to report a new mechanism that regulates specification of lymphocytes, the white blood cells pivotal to immune response. By combining state-of-the art techniques, next-generation deep sequencing and computational data mining, the researchers discovered new epigenetic factors regulating lymphocyte function.
Regulatory regions of the genes studied displayed variations (single nucleotide polymorphisms or SNPs) that have been associated with predisposition to autoimmune diseases such as type1 diabetes, rheumatoid arthritis and inflammatory bowel disease. These discoveries provide new insight into and basis for the study of emergent mechanisms of immune-mediated diseases.
Immune-mediated diseases such as type 1 diabetes, rheumatoid arthritis, asthma and allergies result from abnormal immune response. T lymphocytes that orchestrate the immune response can differentiate into functionally distinct lineages to combat infection and disease. The correct response to cytokines and a controlled balance of T lymphocyte populations are critical for the immune system and for the avoidance of autoimmune disorders.
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The above story is based on materials provided by Suomen Akatemia (Academy of Finland), via AlphaGalileo.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- R. David Hawkins, Antti Larjo, Subhash K. Tripathi, Ulrich Wagner, Ying Luu, Tapio Lönnberg, Sunil K. Raghav, Leonard K. Lee, Riikka Lund, Bing Ren, Harri Lähdesmäki, Riitta Lahesmaa. Global Chromatin State Analysis Reveals Lineage-Specific Enhancers during the Initiation of Human T helper 1 and T helper 2 Cell Polarization. Immunity, 2013; 38 (6): 1271 DOI: 10.1016/j.immuni.2013.05.011
Note: If no author is given, the source is cited instead.
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