Unfortunately, the examination of LRP’s expression and function has been largely confined to human cell lines, mouse cell lines and primary mouse cells. In all these cases a full deletion was not observed, but rather a near complete reduction of LRP. In this study, we show that in the steady state, T cells express low levels of LRP followed by B cells. DCs express a small amount of LRP, but MWs express higher levels of LRP. This demonstrates that on immune cells, LRP expression is largely restricted to phagocytes and professional APCs supporting its role in antigen presentation and modulation of immunity. Because we did not observe changes in iNKT cell activation using single cell suspensions in vitro, but did see a near absence of early iNKT cell IL-4 production following in vivo challenge, we hypothesize that spatial orientation of the LRP expressing macrophages may be important to early iNKT cell responses. We focused our studies on spleen because 1) marginal zone macrophages express receptors that allow them to capture blood borne Niltubacin HDAC inhibitor antigens spleen contains an elaborate distribution network which disseminates molecules present in the blood to white pulp where APCs are located, and 3) iNKT cells that reside in the spleen are exposed to blood borne antigen within minutes after they enter the bloodstream. Our attempts to measure iNKT cell activation in liver and LN shortly after aGC injection were not successful. Therefore, whether iNKT cells in liver and lymph nodes undergo a similar exposure to blood borne antigens is an issue that needs to be addressed in future studies. More recent studies demonstrate that, like the LDLr, other lipid receptors such as scavenger receptor can bind and facilitate uptake of glycolipid antigens by DCs to activate iNKT cells. Preference for receptor/glycolipid interaction was determined to be more dependent on chemical structure of the lipid. Interestingly, both SRA- and LDLr-deficient DCs showed decreased ability to activate the iNKT cell hybridoma DN32.D3 in response to aGC in vitro. However, in vivo challenge of SRA and LDLr-deficient mice with soluble aGC led to the same blunted IL-4 response we observed in LRP-cKO mice. How these receptors contribute to such different cytokine responses remains to be clarified. One possibility is that all three receptors are required for an optimal IL-4 response in vivo. Another may be that loss of any one of these receptors leads to changes in intracellular lipid compositions and that the iNKT cell IL-4 response is sensitive to these changes. Intervention strategies to fully eradicate tuberculosis comprise two main aspects: the prevention of new cases with effective vaccines and the therapeutic treatment of already infected patients. T regulatory cells represent a population of CD4 + T cells whose main function is to control autoimmunity and prevent excessive inflammatory responses that can be detrimental to the host. During infection, Tregs can control immunemediated pathology by negatively regulating effector immune mechanisms against the invading pathogen.