How biological sex shapes differences in immune responses to infection

can influence immune responses and may contribute to sex-specific differences in responses to infection (as reviewed in) [1][2][3].Several genes that are relevant in mediating immune responses to infection that are found on the X chromosome include forkhead box P3 (FOXP3), which inhibits inflammation, interleukin (IL)-2 receptor gamma chain (IL2RG), important for T, B and natural killer cell function, Toll-like receptor (TLR)7 and TLR8, relevant in innate immune function, cluster designation ligand (CD40L), crucial in T cell activation, Bruton's tyrosine kinase (BTK), critical in B cell activation, and C-X-C motif chemokine receptor 3 (CXCR3) which is involved in immune cell migration during inflammatory responses [4,5].In addition, lncRNA XIST has been shown to enhance TLR7-mediated immune activation, which correlates with higher interferon (IFN) signatures and disease activity in females with systemic lupus erythematosus (SLE) [6].Sex hormones and X chromosome-linked genes are not the only contributors to sex differences in the immune response following infection; evidence indicates that epigenetic programming strongly influences immune responses. Epigenetic programming, non-coding RNAs and long-lived immune memory