Immunopharmacology Unit

Abstract About 10% of NSCLCs are mutated in KRAS and impaired in STK11/LKB1, a genetic background associated with poor prognosis, caused by an increase in metastatic burden and resistance to standard therapy. LKB1 is a protein involved in a number of biological processes and is particularly important for its role in the regulation of cell metabolism. LKB1 alterations lead to protein loss that causes mitochondria and metabolic dysfunction that makes cells unable to respond to metabolic stress.

1 Introduction A fascinating aspect of naive CD4+ T cell biology is that the cells can differentiate into specialized subsets that are suited for the resolution of specific categories of inflammation (1). The first of these subsets, Th1 and Th2, were identified from mouse T helper (Th) cell clones, which were found to produce different cytokines when stimulated. Th1 produced IFN-γ, GM-CSF, and IL-3, while Th2 produced IL-3, IL-4, and, at the time, additional unknown factors (2).

In Vitro Differentiated Human CD4 + T Cells Produce Hepatocyte Growth Factor 1University of Copenhagen, Denmark 2Leo Foundation Skin Immunology Research Center, Department of Immunology and Microbiology, Faculty of Health Sciences, University of Copenhagen, Denmark 3Immunopharmacology Unit, Department of Oncology, Mario Negri Pharmacological Research Institute (IRCCS), Italy The final, formatted version of the article will be published soon.