Abstract
A contributing role of nerve growth factor (NGF)-mediated neuroimmunologic mechanisms has provided a new dimension in the understanding of various cutaneous and systemic inflammatory diseases. Recent evidence implicates NGF as a key mediator of inflammation and pain. NGF influences an inflammatory reaction by regulating neuropeptides, angiogenesis, cell trafficking molecules, and T cell activation. All of these functions of NGF are relevant in maintenance or initiation of the critical biologic events in various rheumatologic conditions. The recognition of a pathologic role of NGF and its receptor system has provided an attractive opportunity to develop a novel class of therapeutics for inflammatory diseases and chronic pain syndromes. In this chapter we will discuss the role of NGF and its receptor system in psoriatic disease, inflammatory arthritis, and arthritic pain of osteoarthritis.
| Original language | English (US) |
|---|---|
| Title of host publication | Annals of the New York Academy of Sciences |
| Pages | 470-477 |
| Number of pages | 8 |
| Volume | 1173 |
| DOIs | |
| State | Published - Sep 2009 |
| Externally published | Yes |
Publication series
| Name | Annals of the New York Academy of Sciences |
|---|---|
| Volume | 1173 |
| ISSN (Print) | 00778923 |
| ISSN (Electronic) | 17496632 |
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Keywords
- NGF
- Psoriasis
- Psoriatic arthritis
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
Cite this
NGF and its receptor system : A new dimension in the pathogenesis of psoriasis and psoriatic arthritis. / Raychaudhuri, Smriti K.; Raychaudhuri, Siba P.
Annals of the New York Academy of Sciences. Vol. 1173 2009. p. 470-477 (Annals of the New York Academy of Sciences; Vol. 1173).Research output: Chapter in Book/Report/Conference proceeding › Conference contribution
}
TY - GEN
T1 - NGF and its receptor system
T2 - A new dimension in the pathogenesis of psoriasis and psoriatic arthritis
AU - Raychaudhuri, Smriti K.
AU - Raychaudhuri, Siba P
PY - 2009/9
Y1 - 2009/9
N2 - A contributing role of nerve growth factor (NGF)-mediated neuroimmunologic mechanisms has provided a new dimension in the understanding of various cutaneous and systemic inflammatory diseases. Recent evidence implicates NGF as a key mediator of inflammation and pain. NGF influences an inflammatory reaction by regulating neuropeptides, angiogenesis, cell trafficking molecules, and T cell activation. All of these functions of NGF are relevant in maintenance or initiation of the critical biologic events in various rheumatologic conditions. The recognition of a pathologic role of NGF and its receptor system has provided an attractive opportunity to develop a novel class of therapeutics for inflammatory diseases and chronic pain syndromes. In this chapter we will discuss the role of NGF and its receptor system in psoriatic disease, inflammatory arthritis, and arthritic pain of osteoarthritis.
AB - A contributing role of nerve growth factor (NGF)-mediated neuroimmunologic mechanisms has provided a new dimension in the understanding of various cutaneous and systemic inflammatory diseases. Recent evidence implicates NGF as a key mediator of inflammation and pain. NGF influences an inflammatory reaction by regulating neuropeptides, angiogenesis, cell trafficking molecules, and T cell activation. All of these functions of NGF are relevant in maintenance or initiation of the critical biologic events in various rheumatologic conditions. The recognition of a pathologic role of NGF and its receptor system has provided an attractive opportunity to develop a novel class of therapeutics for inflammatory diseases and chronic pain syndromes. In this chapter we will discuss the role of NGF and its receptor system in psoriatic disease, inflammatory arthritis, and arthritic pain of osteoarthritis.
KW - NGF
KW - Psoriasis
KW - Psoriatic arthritis
UR - http://www.scopus.com/inward/record.url?scp=69949187131&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=69949187131&partnerID=8YFLogxK
U2 - 10.1111/j.1749-6632.2009.04652.x
DO - 10.1111/j.1749-6632.2009.04652.x
M3 - Conference contribution
SN - 9781573317627
VL - 1173
T3 - Annals of the New York Academy of Sciences
SP - 470
EP - 477
BT - Annals of the New York Academy of Sciences
ER -