File:Reticular network formation model.jpg: Difference between revisions
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==Model of Reticular Network Formation== | ==Model of Reticular Network Formation== | ||
# Accumulation of lymphocytes induces alteration of mesenchymal progenitors such that they produce chemokines for further lymphocyte attraction and RF components via the secretion of TNFα or LTα (or related cytokines) and likely also via direct contacts mediated by adhesion molecules and LTα1β2. | # Accumulation of lymphocytes induces alteration of mesenchymal progenitors such that they produce chemokines for further lymphocyte attraction and RF components via the secretion of Tumor necrosis factor-alpha (TNFα) or Lymphotoxin-alpha (LTα) (or related cytokines) and likely also via direct contacts mediated by adhesion molecules and LTα1β2. | ||
# Lymphocytes and differentiated FRCs gradually degrade preexisting matrix, and FRCs weave RF meshwork from the newly produced components. | # Lymphocytes and differentiated FRCs gradually degrade preexisting matrix, and FRCs weave RF meshwork from the newly produced components. | ||
# Mature RN forms and antigen presentation occur on the stromal reticulum. | # Mature RN forms and antigen presentation occur on the stromal reticulum. | ||
* LTα exists as either a secreted homotrimer or heterotrimer molecule | |||
** LTα3 homotrimer signals via TNFR1 and TNFR2 | |||
** LTα1β2 heterotrimer with LTβ on the cell surface signals through the LTβ receptor (LTβR). | |||
*** unique in the TNF superfamily as a biologically active heterotrimer. | |||
* Lymphotoxin (LT) α1β2 induces dimerization rather than trimerization of the LTβ Receptor (LTβR). | |||
* Homotrimeric TNF superfamily ligands signal by inducing trimers of their receptors. | |||
See also PMID 25663676 [http://www.jimmunol.org/content/194/4/1389/F1.expansion.html Figure - Lymph node paracortex fibroblastic reticular cells] | |||
{{Immune Links}} | |||
===Reference=== | ===Reference=== | ||
Latest revision as of 11:03, 23 February 2016
Model of Reticular Network Formation
- Accumulation of lymphocytes induces alteration of mesenchymal progenitors such that they produce chemokines for further lymphocyte attraction and RF components via the secretion of Tumor necrosis factor-alpha (TNFα) or Lymphotoxin-alpha (LTα) (or related cytokines) and likely also via direct contacts mediated by adhesion molecules and LTα1β2.
- Lymphocytes and differentiated FRCs gradually degrade preexisting matrix, and FRCs weave RF meshwork from the newly produced components.
- Mature RN forms and antigen presentation occur on the stromal reticulum.
- LTα exists as either a secreted homotrimer or heterotrimer molecule
- LTα3 homotrimer signals via TNFR1 and TNFR2
- LTα1β2 heterotrimer with LTβ on the cell surface signals through the LTβ receptor (LTβR).
- unique in the TNF superfamily as a biologically active heterotrimer.
- Lymphotoxin (LT) α1β2 induces dimerization rather than trimerization of the LTβ Receptor (LTβR).
- Homotrimeric TNF superfamily ligands signal by inducing trimers of their receptors.
See also PMID 25663676 Figure - Lymph node paracortex fibroblastic reticular cells
Reference
<pubmed>15381731</pubmed>| J Exp Med.
doi: 10.1084/jem.20040254
Copyright
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Figure 8. panel C cropped from full figure and PMID added.
Cite this page: Hill, M.A. (2024, April 19) Embryology Reticular network formation model.jpg. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/File:Reticular_network_formation_model.jpg
- © Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G
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