Plasmodium species are the protozoan parasite responsible for malaria. Symptoms of malaria include fever, malaise, chills, and body aches, which suggest a highly pro-inflammatory state. I investigated the molecular components of the type I IFN and inflammasome pathways that contributed to inflammation during malaria using both in vitro and in vivo mouse model of infection.
Cytosolic DNA sensing pathways are now increasingly implicated in myriad infectious and autoimmune diseases.The identification of bonafide sensors and contributors to this response has been a particular focus of mine. My largest contributions to this field are as yet unpublished works identifying novel players in cytosolic DNA sensing. Much of my work on characterizing DNA-sensing pathways stemmed from the identification of a unique AT-rich motif ubiquitous in the Pf genome that are also over- represented in the genomes of DNA viruses, bacteria and retroelement-derived repeats in mammals. I have since used this motif in a mass-spectrometry based proteomic screen to identify two novel players in the cytosolic DNA-sensing pathway.
The hallmark of autoimmunity is the dramatic loss of immune homeostasis. My research focused on understanding the contribution of the cytosolic DNA-sensing pathway in modulating autoimmunity.
Age-induced changes in immune-homeostasis often result in chronic syndromes associated with age. Osteoporosis/Osteopenia, are hallmarks of age-induced changes, whereby a catabolic shift in bone metabolism has deleterious effects on the host. Intriguingly, modulators of bone homeostasis include osteoblasts (OB) derived from mesenchymal precursors and osteoclasts (OC) derived from myeloid progenitors. OCs utilize immune mechanisms for osteoclastogenic activities and thus, many pathways operative in myeloid cells have direct impact on bone metabolism. My research is focused on understanding the contribution of cytosolic DNA-sensing pathways to bone metabolism with age.
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