Research group Group Gekara

The immune system that kills disease-causing microbes and heals tissues, and the DNA repair system that maintains gene expression are essential for life. However, they require careful regulation to prevent the destruction of own tissues. The goal of my research is to better understand these systems and find new strategies in the treatment of diseases.


Our body depends on two major defense systems for protection against external and internal threats: 1) the immune system which mediates pathogen clearance and tissue healing, and 2) the DNA damage response which senses and repairs DNA breaks thereby ensuring that our genetic material is preserved. While essential for life, if not properly controlled, these surveillance systems can cause havoc. Indeed, dysregulations in the immune and DNA repair systems lie at the core of many health afflictions, including infections, autoimmune/inflammatory diseases, neurodegenerative diseases, cancer, and other age-associated disorders.

The overarching goal of my research is to understand how the innate immune are regulated and DNA repair systems and to identify new strategies for manipulating these systems in disease management. We have made some progress toward this goal and contributed to our understanding of how the immune and DNA repair systems cross-communicate and the regulatory component involved.

Microbes with established coexistence with their hosts have evolved strategies to manipulate host defenses. Another area of my research interest is how microbes including the commensal microbiota and pathogens (bacteria and viruses) modulate the immune and DNA repair pathways and how this impacts disease development. 

The research in my lab focuses on fundamental cell biological processes with the view that some of our discoveries will benefit human health.

This research group has no members.

There are no research project connections.

The gut microbiota prime systemic antiviral immunity via the cGAS-STING-IFN-I axis. - Erttmann SF, Swacha P, Aung KM, Brindefalk B, Jiang H, Härtlova A, Uhlin BE, Wai SN, Gekara NO. (2022). Immunity. 55(5):847-861.e10. doi: 10.1016/j.immuni.2022.04.006.

Nuclear AIM2-Like Receptors Drive Genotoxic Tissue Injury by Inhibiting DNA Repair. - Jiang H, Swacha P, Gekara NO. (2021). Advanced Science. 8(22):e2102534. doi: 10.1002/advs.202102534.

Chromatin-bound cGAS is an inhibitor of DNA repair and hence accelerates genome destabilization and - cell death. Jiang H, Xue X, Panda S, Kawale A, Hooy RM, Liang F, Sohn J, Sung P, Gekara NO. EMBO J. 2019 Sep 23:e102718. doi: 10.15252/embj.2019102718.

Hydrogen peroxide release by bacteria suppresses inflammasome-dependent innate immunity. - Erttmann SF, Gekara NO. Nat Commun. 2019 Aug 2;10(1):3493. doi: 10.1038/s41467-019-11169-x.

The deubiquitinase MYSM1 dampens NOD2-mediated inflammation and tissue damage by inactivating the - RIP2 complex. Panda S, Gekara NO. Nat Commun. 2018 Nov 7;9(1):4654.

Loss of the DNA Damage Repair Kinase ATM Impairs Inflammasome-Dependent Anti-Bacterial Innate - Immunity. Erttmann SF, Härtlova A, Sloniecka M, Raffi FA, Hosseinzadeh A, Edgren T, Rofougaran R, Resch U, Fällman M, Ek T, Gekara NO. Immunity. 2016 Jul 19;45(1):106-18.

Deubiquitinase MYSM1 regulates innate immunity through inactivation of TRAF3 and TRAF6 complexes. - Panda S, Nilsson JA and Gekara NO. Immunity. 2015 Oct 13;43(4).

DNA damage primes the type I interferon system via the cytosolic DNA sensor STING to promote - anti-microbial innate immunity. Härtlova A, Erttmann SF, Raffi FA, Schmalz AM, Resch U, Anugula S, Lienenklaus S, Nilsson LM, Kröger A, Nilsson JA, Ek T, Weiss S, Gekara NO. Immunity. 2015 Feb 17;42(2):332-43.

Mast cells elicit proinflammatory but not type I interferon responses upon activation of TLRs by - bacteria. Dietrich N, Rohde M, Geffers R, Kroeger A, Hauser H, Weiss S and Gekara NO. Proc Natl Acad Sci U S A. 2010 May 11 Vol 107(19):8748-53.

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