Mitochondria as a central hub control immune cell activation and function via alterations in metabolic pathways, mitochondrial transcription and mitochondrial dynamics. We are interested in understanding which signals regulate these adaptations. Our lab has previously shown that a mitochondrial protein, TCAIM (T hell activation inhibitor, mitochondrial), prevents effector T cell differentiation by controlling mitochondrial functions. We are currently investigating (1) the molecular mechanism of TCAIM regulating cellular metabolism through mitochondrial control and (2) how these metabolic and physiological changes in mitochondria affect immune cell function in multiple disease contexts such as infection and bone regeneration.

• Christine Appelt (cell culture, MACS, flow cytometry, western blot, genotyping)
• Zeynep Oktay (Cell biology)
• Julia Stein (Cell biology)
• Christina Iwert (cell culture, FACS, CyTOF, Metabolomics, RNASeq, tansmission electron microscopy)
• Dr. Olufemi Bolaji (Bioinformatics)

• Identification of Gene Markers for the Prediction of Allograft Rejection or Permanent Acceptance [Am J Transplant 2007, 7(5)]
• TCAIM decreases T cell priming capacity of dendritic cells by inhibiting TLR-induced Ca2+ influx and IL-2 production [J Immunol 2015 , 194(7)]
• The mitochondrial protein TCAIM regulates activation of T cells and thereby promotes tolerance induction of allogeneic transplants [Am J Transplant 2014, 14(12)]
• TCAIM controls effector T cell generation by preventing Mitochondria-Endoplasmic Reticulum Contact Site-initiated Cholesterol Biosynthesis [2021, preprint]
• Transient mTOR inhibition rescues 4-1BB CAR-Tregs from tonic signal-induced dysfunction [Nat Commun 2021, 12(1)]