|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
3
|
|
pubmed:dateCreated |
2009-1-21
|
|
pubmed:abstractText |
Autoimmune diseases are marked by the presence of class-switched, high-affinity autoantibodies with pathogenic potential. Costimulation plays an important role in the activation of T cells and the development of T cell-dependent B cell responses. ICOS plays an indispensable role in the development of follicular helper T cells (T(FH) cells), which provide cognate help to germinal center (GC) B cells. We show that the levels of T(FH) cells and GC B cells in two different models of autoimmunity, the New Zealand Black/New Zealand White (NZB/NZW) F(1) mouse model of systemic lupus erythematosus and the collagen-induced arthritis model of rheumatoid arthritis, are dependent on the maintenance of the ICOS/B7RP-1 pathway. Treatment with an anti-B7RP-1 Ab ameliorates disease manifestations and leads to a decrease in T(FH) cells and GC B cells as well as an overall decrease in the frequency of ICOS(+) T cells. Coculture experiments of Ag-primed B cells with CXCR5(+) or CXCR5(-) T cells show that blocking B7RP-1 does not directly impact the production of IgG by B cells. These findings further support the role of ICOS in autoimmunity and suggest that the expansion of the T(FH) cell pool is an important mechanism by which ICOS regulates Ab production.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
AIM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Blocking,
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD80,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/Autoantibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Icos protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Inducible T-Cell Co-Stimulator...,
http://linkedlifedata.com/resource/pubmed/chemical/Inducible T-Cell Co-Stimulator...
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Feb
|
|
pubmed:issn |
1550-6606
|
|
pubmed:author |
|
|
pubmed:issnType |
Electronic
|
|
pubmed:day |
1
|
|
pubmed:volume |
182
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
1421-8
|
|
pubmed:dateRevised |
2011-11-17
|
|
pubmed:meshHeading |
pubmed-meshheading:19155489-Animals,
pubmed-meshheading:19155489-Antibodies, Blocking,
pubmed-meshheading:19155489-Antibodies, Monoclonal,
pubmed-meshheading:19155489-Antigens, CD80,
pubmed-meshheading:19155489-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:19155489-Arthritis, Experimental,
pubmed-meshheading:19155489-Autoantibodies,
pubmed-meshheading:19155489-B-Lymphocytes,
pubmed-meshheading:19155489-Cell Differentiation,
pubmed-meshheading:19155489-Female,
pubmed-meshheading:19155489-Germinal Center,
pubmed-meshheading:19155489-Inducible T-Cell Co-Stimulator Ligand,
pubmed-meshheading:19155489-Inducible T-Cell Co-Stimulator Protein,
pubmed-meshheading:19155489-Lupus Erythematosus, Systemic,
pubmed-meshheading:19155489-Lymphocyte Activation,
pubmed-meshheading:19155489-Male,
pubmed-meshheading:19155489-Mice,
pubmed-meshheading:19155489-Mice, Inbred BALB C,
pubmed-meshheading:19155489-Mice, Inbred DBA,
pubmed-meshheading:19155489-Mice, Inbred NZB,
pubmed-meshheading:19155489-Random Allocation,
pubmed-meshheading:19155489-Signal Transduction,
pubmed-meshheading:19155489-T-Lymphocytes, Helper-Inducer
|
|
pubmed:year |
2009
|
|
pubmed:articleTitle |
B7RP-1 blockade ameliorates autoimmunity through regulation of follicular helper T cells.
|
|
pubmed:affiliation |
Department of Inflammation, Amgen, Inc., Thousand Oaks, CA 91320, USA.
|
|
pubmed:publicationType |
Journal Article
|
