The vertebrate immune system combines a plethora of specific and unspecific mechanisms to defend the body against invading (and coevolving) pathogens. The more diverse the immune response, the broader the spectrum of recognized pathogens. However, a too diverse immune response may also increase the risk of self-reactivity, in humans known as autoimmune diseases. Hints for such a trade-off can be observed at multiple levels in the immune system, but is most apparent at the Major Histocompatibility Complex (MHC). The MHC encodes highly polymorphic molecules that each recognize specific pathogens, but every individual carries only a very limited number of these genes. We are interested in the processes and constraints that increase or limit and thus shape the individual genetic diversity at the MHC. A current focus is the link between MHC diversity and autoimmunity in human populations, but ultimately we are also interested in a broader perspective and are exploring in which ways diversity at the MHC interacts with other immune genes and the genetic background. For this work we are mostly relying on computational tools and approaches.
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