Former Head


Falk Weih
Falk Weih

Postdocs

Ronny Haenold (Provisional Head)

Marc Riemann

Anja Weidemann

PhD Students

Nico Andreas

Christian Engelmann

Ievgen Oleksandrovich Koliesnik

Master Students

Randy Grimlowski

Sravya Sreekantapuram

Staff Scientists

Debra Weih (histology)

Engineers

Anne Gompf

Technicians

Elke Meier

Heike Dittmar



 

Weih Research Group

Immunology

 

weih_1

 

 

 

 

 

 

We announce with deep sorrow the passing of our group leader, colleague and friend Prof. Dr. Falk Weih, who lost his two-year battle with cancer at the age of 54 on 28 October 2014.

 

Falk has significantly influenced the scientific focus of the FLI. His most important scientific achievements lay in the delineation of molecular mechanisms that play a role in the development of the immune system as well as in the genesis of age-related immune deficiencies. To honor his scientific heritage the Weih group has organized a "Symposium on Molecular Signaling in Health and Disease", which was held on January 16, 2015.

 

With the death of Falk Weih the group now is provisionally headed by senior scientist Ronny Haenold.

 

 

 

 

 

 

 

 

The NF-κB signal transduction pathway in development and dysfunction of the immune system

The Rel/NF-κB transcription factors play a pivotal role in immune responses, inflammation/autoimmunity, the regulation of apoptosis, and in cancer. With the help of genetically altered mouse models we are analyzing the NF-κB signaling pathway in both normal development and pathological alterations of the immune system, focusing on the recently described alternative activation pathway. One of our goals is a better understanding of NF-κB function in age-related immune deficiencies and disease.

 

Activation of NF-κB by the alternative (left)

 

Figure 1. Activation of NF-κB by the alternative (left) and the classical pathway (right). Signaling through TNFR, IL-1R, or Toll-like receptors (TLR) activates the classical NF-κB pathway involving predominantly the β and γ subunits of the IKK complex. Nuclear translocation and DNA-binding of p50-RelA heterodimers is accomplished through IκBα phosphorylation and ubiquitin-dependent proteasomal degradation. Membrane-bound LTα1β2, CD40, and BAFF, on the other hand, activate via their respective receptors the kinases NIK and IKKα. Phosphorylation of p100 results in the processing of the precursor to the p52 subunit and nuclear accumulation of p52-RelB heterodimers. There is significant cross talk since signaling through the LTβR, for instance, also results in the induction of RelA complexes. It is believed that the two pathways activate distinct sets of genes.

 

 

 

 

 

 

 

 

Projects

  • Regulation of lymphoid organ development by the NF-κB signaling pathway
  • Development and function of natural killer T cells, γδ T cells and dendritic cells
  • Regulation of early B cell development by NF-κB
  • Regulation of adipogenesis by NF-κB
  • Tertiary lymphoid organs in atherosclerosis
  • Transcriptional control of neuronal plasticity and neurosenescence by NF-κB

 

Recent selected publications

  • Haenold R, Weih F, Herrmann KH, Schmidt KF, Krempler K, Engelmann C, Nave KA, Reichenbach JR, Löwel S, Witte OW, Kretz A. (2014) NF-κB controls axonal regeneration and degeneration through cell-specific balance of RelA and p50 in the adult CNS. J Cell Sci, 127, 3052-3065. [PubMed]
  • Fischer S, Engelmann C, Herrmann KH, Reichenbach JR, Witte OW, Weih F, Kretz A, Haenold R. (2014) In vivo imaging of optic nerve fiber integrity by contrast-enhanced MRI in mice. J Vis Exp, (89), doi: 10.3791/51274. [PubMed]
  • Krljanac B, Weih D, Jacobsen ID, Hu D, Koliesnik I, Reppe K, Witzenrath M, Weih F. (2014) NF-κB2/p100 deficiency impairs immune responses to T-cell-independent type 2 antigens. Eur J Immunol, 44, 662-672. [PubMed]
  • Kretz A, Herrmann KH, Fischer S, Engelmann C, Witte OW, Reichenbach JR, Weih F, Haenold R. (2014) Dysfunctional NF-κB and brain myelin formation. Eur J Hum Genet, 22, 724-725. [PubMed]
  • Lovas A, Weidemann A, Albrecht D, Wiechert L, Weih D, Weih F. (2012) p100 Deficiency is insufficient for full activation of the alternative NF-κB pathway: TNF cooperates with p52-RelB in target gene transcription. PLoS One, 7, e42741. [PubMed]

 

Recent selected reviews

  • Engelmann C, Weih F, Haenold R. (2014) Role of nuclear factor kappa B in central nervous system regeneration. Neural Regen Res, 9, 707-711. [PubMed]
  • Mohanta SK, Yin C, Peng L, Srikakulapu P, Bontha V, Hu D, Weih F, Weber C, Gerdes N, Habenicht AJ. (2014) Artery tertiary lymphoid organs contribute to innate and adaptive immune responses in advanced mouse atherosclerosis. Circ Res, 114, 1772-1787. [PubMed]
  • Haenold R. (2014) Manganese-enhanced MRI: In vivo imaging of CNS anatomy, fiber connectivity and functional activity. In: In vivo Imaging: New Research, S. 123-153. Editors: R. Hough and J. Camarillo, Nova Science Publishers, Inc., ISBN: 978-1-62948-633-8. [Publisher]
  • Haenold R, Kretz A, Weih F. (2013) Role of NF-κB in neurodegenerative diseases. Forum on Immunopathological Diseases and Therapeutics, 4, 161-179. [Journal]
  • Weih F, Gräbner R, Hu D, Beer M, Habenicht AJ. (2012) Control of dichotomic innate and adaptive immune responses by artery tertiary lymphoid organs in atherosclerosis. Front Physiol, 3, 226. [PubMed]

 


Last update: February 20, 2015

top of the page