 |
MR Vol.12 No.2 indexに戻る
 |
MODERN RHEUMATOLOGY
Vol.12 No.2 |
 |
|
|
 |
|
|
Exploring the signalling pathways promoting T
cell effector responses in chronic inflammation |
|
|
| P. Isomaki1, J. M. Clark1, P. Vagenas1,
A. P. Cope1 |
| (1)Kennedy Institute of Rheumatology Division,
Imperial College School of Medicine, Arthritis Research Campaign
Building, 1 Aspenlea Road, Hammersmith, London W6 8LH, UK |
| |
| Abstract |
| Abstract Over the last decade, it has become
clear that T helper cell differentiation is determined by a programme
of gene transcription, which is in turn dictated by signalling
pathways emanating from both T cell antigen receptors and cytokine
receptors. This model has provided an experimental framework for
exploring the molecular mechanisms through which T cell effector
responses initiate autoimmunity, chronic inflammatory disease,
and allergy. Much less clear are the processes that regulate T
helper cell differentiation and effector responses in established
chronic inflammatory diseases such as rheumatoid arthritis. This
review describes recent experimental data which suggest that the
inflammatory process profoundly influences T cell receptor and
cytokine signal transduction pathways in such a way as to attenuate
both immunoregulatory and host defence mechanisms on the one hand,
while promoting cell survival and effector responses on the other.
These findings are consistent with a model in which the inflammatory
response is initiated primarily by antigen-driven T cell effector
responses, while the chronic phase of the disease process is sustained
by cytokine-driven effector responses. |
| |
| Key words |
| Key words Cytokines ・ Inflammation ・ T cell activation
・ Tumour necrosis factor alpha (TNF) |
|
|
 |
|
|
