Tumor necrosis factor superfamily: Difference between revisions
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{{Short description|A family of cytokines that can cause cell death}} | |||
{{Use dmy dates|date=October 2023}} | |||
[[File:Mouse Tumor Necrosis Factor Alpha.png|thumb|right|Mouse Tumor Necrosis Factor Alpha]] | |||
[[File:PDB 1du3 EBI.jpg|thumb|right|Crystal structure of a TNF receptor]] | |||
The '''tumor necrosis factor superfamily''' (TNFSF) is a group of cytokines that can cause cell death (apoptosis). These cytokines are involved in various cellular processes such as immune system regulation and inflammation. Members of this superfamily are characterized by their ability to bind to specific receptors, known as tumor necrosis factor receptors (TNFRs), which trigger signaling pathways leading to diverse cellular responses. | |||
==Structure== | ==Structure== | ||
The TNF superfamily members are typically type II transmembrane proteins, although some can be cleaved to form soluble cytokines. They share a common structural motif known as the TNF homology domain, which is crucial for receptor binding. The receptors for these cytokines are type I transmembrane proteins that contain cysteine-rich domains in their extracellular regions, which are important for ligand binding. | |||
==Function== | ==Function== | ||
The | The primary role of TNFSF members is to regulate immune responses and inflammation. They are involved in the activation, proliferation, and differentiation of immune cells. For example, [[tumor necrosis factor alpha]] (TNF-_) is a key mediator of inflammation and is involved in the pathogenesis of various inflammatory diseases such as rheumatoid arthritis and inflammatory bowel disease. | ||
== | ==Members== | ||
The | The TNF superfamily includes several well-known cytokines, such as: | ||
* [[Tumor necrosis factor alpha]] (TNF-_) | |||
* [[Fas ligand]] (FasL) | |||
* [[CD40 ligand]] (CD40L) | |||
* [[RANK ligand]] (RANKL) | |||
Each of these cytokines interacts with specific receptors to mediate distinct biological effects. For instance, FasL binds to the Fas receptor to induce apoptosis, while CD40L interacts with CD40 to promote B cell activation and antibody production. | |||
==Clinical Significance== | ==Clinical Significance== | ||
Dysregulation of | Dysregulation of TNFSF members and their receptors is associated with a variety of diseases, including autoimmune disorders, cancer, and infectious diseases. Therapeutic agents targeting TNF-_, such as monoclonal antibodies and receptor antagonists, have been developed to treat inflammatory conditions like rheumatoid arthritis and Crohn's disease. | ||
==Research | ==Research== | ||
Ongoing research is focused on understanding the complex signaling pathways mediated by TNFSF members and their potential as therapeutic targets. Structural studies, such as those using [[X-ray crystallography]], have provided insights into the interactions between TNFSF cytokines and their receptors, aiding in the design of novel drugs. | |||
== | ==Related pages== | ||
* [[Cytokine]] | * [[Cytokine]] | ||
* [[Apoptosis]] | * [[Apoptosis]] | ||
* [[Inflammation]] | * [[Inflammation]] | ||
[[Category:Cytokines]] | [[Category:Cytokines]] | ||
[[Category:Immune system]] | |||
Revision as of 20:54, 9 February 2025
A family of cytokines that can cause cell death
The tumor necrosis factor superfamily (TNFSF) is a group of cytokines that can cause cell death (apoptosis). These cytokines are involved in various cellular processes such as immune system regulation and inflammation. Members of this superfamily are characterized by their ability to bind to specific receptors, known as tumor necrosis factor receptors (TNFRs), which trigger signaling pathways leading to diverse cellular responses.
Structure
The TNF superfamily members are typically type II transmembrane proteins, although some can be cleaved to form soluble cytokines. They share a common structural motif known as the TNF homology domain, which is crucial for receptor binding. The receptors for these cytokines are type I transmembrane proteins that contain cysteine-rich domains in their extracellular regions, which are important for ligand binding.
Function
The primary role of TNFSF members is to regulate immune responses and inflammation. They are involved in the activation, proliferation, and differentiation of immune cells. For example, tumor necrosis factor alpha (TNF-_) is a key mediator of inflammation and is involved in the pathogenesis of various inflammatory diseases such as rheumatoid arthritis and inflammatory bowel disease.
Members
The TNF superfamily includes several well-known cytokines, such as:
- Tumor necrosis factor alpha (TNF-_)
- Fas ligand (FasL)
- CD40 ligand (CD40L)
- RANK ligand (RANKL)
Each of these cytokines interacts with specific receptors to mediate distinct biological effects. For instance, FasL binds to the Fas receptor to induce apoptosis, while CD40L interacts with CD40 to promote B cell activation and antibody production.
Clinical Significance
Dysregulation of TNFSF members and their receptors is associated with a variety of diseases, including autoimmune disorders, cancer, and infectious diseases. Therapeutic agents targeting TNF-_, such as monoclonal antibodies and receptor antagonists, have been developed to treat inflammatory conditions like rheumatoid arthritis and Crohn's disease.
Research
Ongoing research is focused on understanding the complex signaling pathways mediated by TNFSF members and their potential as therapeutic targets. Structural studies, such as those using X-ray crystallography, have provided insights into the interactions between TNFSF cytokines and their receptors, aiding in the design of novel drugs.
