Suppression of inflammation and joint destruction in rheumatoid arthritis may require a concerted action of Th2 cytokines.
A predominance of T-helper 1 (Th1) activity and a lack of Th2 activity has been documented in the inflamed joints of patients with rheumatoid arthritis (RA). This imbalance is suggested to contribute to activation of, particularly, inflammatory macrophages and B-cells. Th2-mediated immunity, like atopy, is associated with amelioriated inflammation and joint damage in RA patients. Despite the potent anti-inflammatory capacities of two prominent Th2 cytokines in many experimental studies, clinical trials with either human IL-4 or IL-10 in RA patients did not lead to substantial disease suppression. Based on a thorough evaluation of the actions of IL-4 and IL-10 in these studies, it is hypothesized that disease suppression of RA may require the concerted action of suppressive Th2 cytokines or Th2 activity.
van Roon
Joel A G
JA
Department of Rheumatology & Clinical Immunology, University Medical Center Utrecht, The Netherlands. J.vanRoon@azu.nl
Bijlsma
Johannes W J
JW
Lafeber
Floris P J G
FP
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism* / Q000473:pathology*; D016207:Cytokines / Q000819:agonists / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000517:prevention & control; D016753:Interleukin-10 / Q000819:agonists / Q000276:immunology / Q000378:metabolism; D015847:Interleukin-4 / Q000819:agonists / Q000276:immunology / Q000378:metabolism; D018418:Th2 Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*
D016207:Cytokines; D016753:Interleukin-10; D015847:Interleukin-4