Autoimmune diseases occur when an individual's immune system fights their own body as if it was a foreign invader. However, in healthy people, these responses are prevented by a process known as immune tolerance. Many complex biological mechanisms maintain the necessary balance between immune activation and suppression to ensure immune tolerance does not prevent the body from effectively fighting pathogens. n a new study published in PNAS, a group of researchers from the University of Tsukuba uncovered how the relationship between two receptors called DNAM-1 and TIGIT helps preserve the balance for optimal immune function. Both of these molecules have previously been studied in a subset of immune cells called regulatory T cells, or Tregs.

Tregs are crucial mediators of immune tolerance and autoimmunity prevention. Treg activity is typically inhibited during inflammatory reactions to infection to allow the body to efficiently fight and clear the invader. However, the molecular mechanisms that control this balance in Treg behaviour are not fully understood. When a specific activating molecule (CD155) binds to the receptors DNAM-1 and TIGIT, they trigger signals that tell the T cells how to behave and what functions to perform.

The Tsukuba team found that DNAM-1 and TGIT compete for CD155 under inflammatory conditions. When CD155 binds to DNAM-1, this receptor sends messages that tell the immune system to wake up and activate. However, when CD155 binds to TIGIT, this receptor acts the opposite way and suppresses the immune system, thereby telling the T cells to stop activating.

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John
Editorial Assistant
Immunogenetics Open Access