My research is focused on the improvement of a neutrophil-targeting, bi-specific antibody therapy for cancers by the addition of an immuno-active payload to the antibody. 

Seeing as they constitute 60 to 70% of all circulating leukocytes, neutrophils are criminally underrated and underused in the development of immune therapies. Especially since they've been proven to be capable of Antibody-Dependent Cellular Cytotoxicity (ADCC) of tumor cells via a mechanism known as trogocytosis or frustrated phagocytosis, where they quite literally rip the tumor cells apart. An important fact to mention is that neutrophils are only strongly activated by antibodies of the IgA isotype, which is never used in therapies due to it having a very short half-life in patients.
We've developed a new, promising antibody therapy that is able to strongly activate neutrophils whilst retaining the long half-life associated with regular antibody therapies. However, in testing this antibody we noticed an interesting phenomenon. Innate immune cells were being recruited to the tumor, but were unable to infiltrate into it. 
My research investigates methods to improve upon this promising antibody therapy by adding an immuno-active payload to the antibody, creating an immunocytokine. This immuno-active payload can be any of the tens of cytokines or chemokines described in literature. And seeing as every cyto- or chemokine has a very distinct effect on the immune system, we are able to very specifically skew the immune response to our therapy.