Project Details
Projekt
FOR 876: Mechanisms Dampening Inflammation
Subject Area
Medicine
Term
from 2007 to 2011
Project identifier
Deutsche Forschungsgemeinschaft (DFG) - Project number 34814745
Inflammation is a fundamental and ubiquitous reaction of higher organisms to trauma and infection. The purpose of the inflammatory reaction is to eliminate injured tissues and foreign invaders and to restore the structural and functional integrity of tissues and organs. Therefore, inflammation can be considered as a key element for the preservation of tissue homeostasis.
The inflammatory process consists of many coordinated pathophysiological steps such as changes in the local blood circulation, infiltration, accumulation and activation of different cell types at the traumatised tissue site, removal of pathogenic organisms, debris and in-flammatory cells and finally tissue repair. The quality and quantity of the injury and the type of affected tissue or organ determine the nature of the particular inflammatory reactions.
Normally, after termination of the inflammatory process tissue and organ functions are restored. However, in cases when the balance between inflammatory reaction and resolution is disturbed, self-destructive chronic inflammation may develop resulting in defective or loss of organ functions. Due to the dilemma of the absolute requirement of an inflammatory reaction for effective immune defense, on the one hand, and potential tissue destruction due to the inflammatory reaction, on the other hand, tight regulation of this process is necessary.
Inflammation, the immediate immunological consequence of recognition of pathogenic material by the immune system, is considered a necessary, initial component of innate as well as adaptive immunity. Inflammation constitutes a relevant accompaniment of both the humoral as well as the cellular immune response. However, excessive or prolonged inflammatory responses can themselves cause considerable tissue and organ damage. Complete inhibition of the inflammatory reaction would leave the organism immune compromised and, therefore, unable to mount an effective immune defense. Consequently, simultaneously with the initiation of an acute inflammatory reaction a coordinated programme is initiated, aimed at fine tuning the degree of the immune reaction sufficient for resolution of inflammation. Accordingly, multiple tightly controlled inhibitory mechanisms selective for individual cellular and molecular reactions of the immune response are required to restore immune homeostasis and permit the development of an adequate immune reaction upon renewed stimulation.
The aim of this Research Unit is the detailed analysis of specific immune regulatory mechanisms to disclose possibilities for therapeutic interventions dampening inflammation.
The inflammatory process consists of many coordinated pathophysiological steps such as changes in the local blood circulation, infiltration, accumulation and activation of different cell types at the traumatised tissue site, removal of pathogenic organisms, debris and in-flammatory cells and finally tissue repair. The quality and quantity of the injury and the type of affected tissue or organ determine the nature of the particular inflammatory reactions.
Normally, after termination of the inflammatory process tissue and organ functions are restored. However, in cases when the balance between inflammatory reaction and resolution is disturbed, self-destructive chronic inflammation may develop resulting in defective or loss of organ functions. Due to the dilemma of the absolute requirement of an inflammatory reaction for effective immune defense, on the one hand, and potential tissue destruction due to the inflammatory reaction, on the other hand, tight regulation of this process is necessary.
Inflammation, the immediate immunological consequence of recognition of pathogenic material by the immune system, is considered a necessary, initial component of innate as well as adaptive immunity. Inflammation constitutes a relevant accompaniment of both the humoral as well as the cellular immune response. However, excessive or prolonged inflammatory responses can themselves cause considerable tissue and organ damage. Complete inhibition of the inflammatory reaction would leave the organism immune compromised and, therefore, unable to mount an effective immune defense. Consequently, simultaneously with the initiation of an acute inflammatory reaction a coordinated programme is initiated, aimed at fine tuning the degree of the immune reaction sufficient for resolution of inflammation. Accordingly, multiple tightly controlled inhibitory mechanisms selective for individual cellular and molecular reactions of the immune response are required to restore immune homeostasis and permit the development of an adequate immune reaction upon renewed stimulation.
The aim of this Research Unit is the detailed analysis of specific immune regulatory mechanisms to disclose possibilities for therapeutic interventions dampening inflammation.
DFG Programme
Research Units
Projects
- Analysis of TNFR1 internalization-dependent TNF-mediated resolution of the inflammatory response (Applicant Schneider, Wulf )
- Functional Characterization of Lymphotoxin-beta-Rezeptor Activation in Inflammation (Applicant Hehlgans, Thomas )
- Influence of the pattern recognition receptor TLR5 on GVHD and the protective effect of donor CD4+CD25+ regulatory T cells following allogeneic bone marrow transplantation (Applicant Hoffmann, Petra )
- Koordination der Forschungsgruppe 876 (Applicant Männel, Daniela N. )
- Role of TNFR2 in sepsis-induced immune suppression (Applicant Männel, Daniela N. )
- The role of integrin alphaE-positive intestinal dendritic cells in inflammatory processes within the gut and their involvement in tolerance (Applicant Strauch, Ulrike Gisela )
- The role of T cell SMAD7 in cellular immunity and in the regulation of autoimmune inflammation in the central nervous system (Applicant Kleiter, Ingo )
Spokesperson
Professorin Dr. Daniela N. Männel
