In vivo administration of recombinant CD155 protein resulted in a delayed development of SLE in MRL/lpr mice by impairing the activity of CD4+ T cells, including the expression of CD25, and CD69, production of IFN-γ, and proliferation, this data shows that activation of the TIGIT pathway can down‐regulate the activities of CD4+ T cells which reveals a new method to treat SLE (79). Here, CD69 is linked to systemic lupus erythematosus.