Abstract
Lymphocyte costimulation via the inducible costimulatory molecule (ICOS) is required for effective humoral immunity development. Following immunization with Torpedo acetylcholine receptor (AChR), ICOS gene knockout (KO) mice were highly resistant to clinical experimental autoimmune myasthenia gravis (EAMG) development, had less serum AChR-specific immunoglobulins (Igs), and exhibited a diminutive germinal center (GC) reaction in secondary lymphoid tissues. Lymphocyte proliferation and both Th1 and Th2 differentiation in response to AChR and the AChR dominant α146-162 peptide were inhibited by the ICOS gene deficiency. ICOS-mediated lymphocyte costimulation is thus vital to the induction of T cell-mediated humoral immunity to AChR and the development of clinical EAMG.
Original language | English (US) |
---|---|
Pages (from-to) | 16-25 |
Number of pages | 10 |
Journal | Journal of Neuroimmunology |
Volume | 153 |
Issue number | 1-2 |
DOIs | |
State | Published - Aug 2004 |
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Keywords
- α-bungarotoxin
- Ab
- acetylcholine receptor
- AChR
- antibody
- antigen presenting cell
- APC
- Autoimmunity
- B7RP-1
- BTX
- Costimulation
- EAMG
- Experimental autoimmune myasthenia gravis
- experimental autoimmune myasthenia gravis
- ICOS
- Ig
- Myasthenia gravis
ASJC Scopus subject areas
- Immunology
- Clinical Neurology
- Immunology and Allergy
- Neurology
Cite this
ICOS is essential for the development of experimental autoimmune myasthenia gravis. / Scott, Benjamin G.; Yang, Huan; Tüzün, Erdem; Dong, Chen; Flavell, Richard A.; Christadoss, Premkumar.
In: Journal of Neuroimmunology, Vol. 153, No. 1-2, 08.2004, p. 16-25.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - ICOS is essential for the development of experimental autoimmune myasthenia gravis
AU - Scott, Benjamin G.
AU - Yang, Huan
AU - Tüzün, Erdem
AU - Dong, Chen
AU - Flavell, Richard A.
AU - Christadoss, Premkumar
PY - 2004/8
Y1 - 2004/8
N2 - Lymphocyte costimulation via the inducible costimulatory molecule (ICOS) is required for effective humoral immunity development. Following immunization with Torpedo acetylcholine receptor (AChR), ICOS gene knockout (KO) mice were highly resistant to clinical experimental autoimmune myasthenia gravis (EAMG) development, had less serum AChR-specific immunoglobulins (Igs), and exhibited a diminutive germinal center (GC) reaction in secondary lymphoid tissues. Lymphocyte proliferation and both Th1 and Th2 differentiation in response to AChR and the AChR dominant α146-162 peptide were inhibited by the ICOS gene deficiency. ICOS-mediated lymphocyte costimulation is thus vital to the induction of T cell-mediated humoral immunity to AChR and the development of clinical EAMG.
AB - Lymphocyte costimulation via the inducible costimulatory molecule (ICOS) is required for effective humoral immunity development. Following immunization with Torpedo acetylcholine receptor (AChR), ICOS gene knockout (KO) mice were highly resistant to clinical experimental autoimmune myasthenia gravis (EAMG) development, had less serum AChR-specific immunoglobulins (Igs), and exhibited a diminutive germinal center (GC) reaction in secondary lymphoid tissues. Lymphocyte proliferation and both Th1 and Th2 differentiation in response to AChR and the AChR dominant α146-162 peptide were inhibited by the ICOS gene deficiency. ICOS-mediated lymphocyte costimulation is thus vital to the induction of T cell-mediated humoral immunity to AChR and the development of clinical EAMG.
KW - α-bungarotoxin
KW - Ab
KW - acetylcholine receptor
KW - AChR
KW - antibody
KW - antigen presenting cell
KW - APC
KW - Autoimmunity
KW - B7RP-1
KW - BTX
KW - Costimulation
KW - EAMG
KW - Experimental autoimmune myasthenia gravis
KW - experimental autoimmune myasthenia gravis
KW - ICOS
KW - Ig
KW - Myasthenia gravis
UR - http://www.scopus.com/inward/record.url?scp=3242721247&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=3242721247&partnerID=8YFLogxK
U2 - 10.1016/j.jneuroim.2004.04.019
DO - 10.1016/j.jneuroim.2004.04.019
M3 - Article
C2 - 15265659
AN - SCOPUS:3242721247
VL - 153
SP - 16
EP - 25
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
SN - 0165-5728
IS - 1-2
ER -