Based on these other models, we hypothesized that the Ly6Clo, CX3CR1+ monocytes would migrate into brain towards CX3CL1 and play an important role in functional recovery after ICH at sub-acute time points. Our results suggest that CX3CR1 on monocytes does not play an influential role in acute inflammation or functional recovery after ICH. Rather, Similar between the genotypes that it is unlikely any difference that might exist would have any meaningful impact. Therefore we conclude there is no role for the chemokine receptor in functional outcomes after ICH. We used the whole blood injection model in this work, and a limitation of this model is that the initial neurological deficit after ICH is not as severe as in the collagenase model. However, the introduction of bacterial collagenase into the brain parenchyma may result in inflammation due to the presence of a foreign antigen in the brain, which is not a concern with the blood injection model. Women exhibit differences in Toll-like receptor 7 responsiveness, T regulatory cell activity, and environmental factor exposure compared to men. These differences may account for the stronger cellular and humoral immune responses in women, as well as their higher risk of autoimmune diseases. Systemic lupus erythematosus occurs primarily in women at a ratio compared to men. Although host immune factors, epigenetic and environmental factors may partially account for the higher prevalence of SLE in women, the exact mechanisms are not fully understood. The onset of SLE disease most often occurs in women during the child-bearing years, therefore sex hormones are believed to play a major role in the etiology of SLE disease. In the periphery, plasmacytoid dendritic cells, as well as other immune cells, express estrogen receptor alpha, pDCs play an important role in SLE disease pathogenesis due to their function in mediating immune responses as well as their producing large amounts of IFN-a in response to TLR7 and TLR9 ligands Knockout of ERa in both control and lupus prone mouse strains resulted in reduced TLR3, TLR4, TLR7 and TLR9 responses in pDCs, spleen cells and B cells, suggesting that estrogen signaling affects TLR responsiveness. Guery’s group showed that pre-menopausal, not post-menopausal women, have kinase inhibitors increased pDC responses to TLR ligands compared to men through a cell-intrinsic ERa signaling. Being located on the X chromosome, TLR7 responsiveness, as shown in IFN-a production, in pDCs from women is higher than men. Given that women possess have two TLR7 genes, compared to the one in men, led to speculation that epigenetic factors/X chromosome inactivation issues may partially explain enhanced female responsiveness to TLR7 agonists. Treatments targeting TLR7/8 and TLR9 are in Phase I trials in patients with SLE and should provide insight into the role of TLR signaling in lupus including whether these therapies will be more effective in women than men. Other immune cells have variable ER expression. B cells express ERb, CD4 T cells express ERa, CD8 T cells and monocytes may express low levels of both ERs.