Corneth, Odilia B J <br/><br/>
Absence of interleukin-17 receptor a signaling prevents autoimmune inflammation of the joint and leads to a Th2-like phenotype in collagen-induced arthritis.  [electronic resource] 

 -  Arthritis & rheumatology (Hoboken, N.J.)  Feb 2014 
 - 340-9 p.  digital 
<br/><br/> Publication Type: Journal Article 
<br/><br/><label>ISSN: </label>2326-5205 
<br/><br/><label>Standard No.: </label>10.1002/art.38229  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Animals<br/>Arthritis, Experimental--pathology<br/>Autoimmune Diseases--physiopathology<br/>CD4-Positive T-Lymphocytes--metabolism<br/>Disease Models, Animal<br/>Inflammation--physiopathology<br/>Interleukin-17--metabolism<br/>Interleukin-23 Subunit p19--deficiency<br/>Interleukin-4--metabolism<br/>Joints--pathology<br/>Mice<br/>Mice, Inbred C57BL<br/>Mice, Knockout<br/>Phenotype<br/>Plasma Cells--pathology<br/>Receptors, Interleukin-17--deficiency<br/>Severity of Illness Index<br/>Signal Transduction--physiology<br/>Th2 Cells--pathology