Hypothesis
Influence of hypoxia in inflammatory synovitis
| The first 150 words of the full text of this article appear below. |
Hypothesis
Persistent synovitis results from a hypoxia driven progressive transition to glycolytic metabolism that promotes transcriptional changes permissive to unresolved inflammation as the disease progresses. Erosion of cartilage and bone may involve gene expression characteristic to the "anoxic response system" of wound repair.
HYPOXIA AND MODULATION OF IMMUNE RESPONSES
The pathogenesis of rheumatoid arthritis (RA) is hypothesised to
involve inappropriate triggering of the MHC controlled immune surveillance, resulting in altered T and B cell profiles. Recently, the
cytokine profile of T helper lymphocytes has been associated with the
disease. The cytokine repertoire of inflamed synovia is categorised as
that of a Th1 response. The characteristic Th1 response displays
increased expression of select cytokines such as TGF
, IFN
,
TNF
, IL1, and IL2. In contrast, Th2 responses exhibit increased IL4,
IL5, IL10, and IL13 (predominantly anti-inflammatory cytokines). While
the levels of TNF and IL1 are high within RA synovium,1
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