Cellular and Molecular Neuroimmunology Group (Head Dr. T. Blank)
We are interested in the complex interactions between the immune and nervous system. Until very recently, scientists assumed that any activity of the immune system within or around the central nervous system (CNS) was a hallmark of pathology. However, other lines of evidence support the notion that immune support is actually required for optimal neuronal function during development and adulthood and might otherwise lead to disorders like depression, anxiety, schizophrenia, OCD or cognitive impairment.
Personalia
| Dr. Thomas Blank | Principal Investigator | +49-761-270-50640 |
| Dr. Adam Gregory Peres | Postdoc | +49-761-270-51110 |
| Omar Mossad | PhD Student | +49-761-270-93380 |
| Feres Mocayar | cand. med. | +49-761-270-52800 |
| Franziska Kessler | cand. med. | +49-761-270-51100 |
| Lara Nabavi | cand. med. | +49-761-270-51100 |
| Melanie Mayer | visit. student | +49-761-270-51100 |
| Marius Schwabenland | MD (AG Prinz) | +49-761-270-50640 |
Research Topics
Impact of Interferons on CNS function
It has become evident that the generalized perception of the brain and spinal cord as 'immune-privileged sites' need to be revisited; circulating leukocytes were shown to play an indispensable role in maintenance and repair of the CNS. Accordingly, immune-deficient mice or mice with increased immune response are more susceptible to mental stress, suffer from cognitive deficits, and show reduced hippocampal neurogenesis levels when compared to their wild-type counterparts. Also, interferons itself affect cells in the CNS, which can be transient or long-lasting. It is the main focus of our ongoing research to further understand the direct or indirect impact of interferons on CNS function.
Contributionof microglia to brain function and development
Microglia are highly ramified cells that have a multitude of fine, exceptionally motile processes that continuously survey the parenchymal environment. Through this surveillance, microglia detect diverse extracellular signals, and consequently, transduce, integrate and respond to them to maintain brain homeostasis. It is increasingly appreciated that many of the response states of microglia are distinctly different from CNS activation during immune responses and are crucial for normal brain development and homeostasis. Thus, in contrast to the roles they have had attributed to them in the past, microglia are known to be active participants in brain function and dysfunction and represent one of the main target cells of our present research.
Fig.: Interaction of activated microglia (lba1/CD68) with immature neurons (DCX) (left) and respective 3D reconstruction (right).
References
Blank T., Goldman T. and Prinz M. (2014) Microglia fuel the learning brain. Trends Immunol. 4:139-140.
Blank T., Detje C.N., Spieß A., Hagemeyer N., Brendecke S.M., Wolfart J., Staszewski O., Zöller T., Papageorgiou I., Schneider J., Paricio-Montesinos R., Eisel U.L.M., Manahan-Vaughan D., Jansen S., Lienenklaus S., Lu B., Imai Y., Müller M., Goelz S.E., Baker D.P., Schwanninger M. Kann O., Heikenwälder M., Kalinke U. and Prinz M. (2016) Brain endothelial and epithelial specific IFNAR is key for virus-induced sickness behavior and cognitive impairment. Immunity 44:901-912.
Blank T. and Prinz M. (2017) Type I interferon pathway in CNS homeostasis and neurological disorders. Glia 65:1397-1406
Mass E., Jacome-Galarza C.E.*, Blank T.*, Lazarov T., Durham B.H., Ozkaya N., Pastore A., Schwabenland M., Chung Y.R., Rosenblum M.K., Prinz M., Abdel-Wahab O. and Geissmann F. (2017) A somatic mutation in erythro-myeloid progenitors causes neurodegenerative diseases. Nature 549:389-393
Wendeln A.C., Degenhardt K., Kaurani L., Gertig M., Ulas T., Jain G., Wagner J., Häsler L.M., Wild K., Skodras A., Blank T., et al. (2018) Innate immune memory in the brain shapes neurological disease hallmarks. Nature 556:332-338.
Blank T.*, Goldmann T.*, Koch M., Amann L., Schön C., Bonin M., Pang S., Prinz M., Burnet M., Wagner J., Biel M. and Michalakis S. (2018) Early microglia activation precedes photoreceptor degeneration in a mouse model of CNGB1-linked retinitis pigmentosa. Front Immunol. 8:1930
