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Section for Medical Inflammation Research, University of Lund, Lund, Sweden
IL-10 is a pleiotropic cytokine with stimulatory and inhibitory
properties, and is thought to have a protective role in rheumatoid
arthritis and collagen-induced arthritis (CIA). In this study, we
investigated how IL-10 deficiency affects CIA and anti-collagen
type II (CII) Ab-transferred arthritis in C57BL/10.Q (B10.Q) mice. The
B10.Q.IL-10-/- mice had an 8-cM 129/Ola fragment around
the IL-10 gene. The mice were treated with antibiotics, appeared
healthy, and had no colitis. T cells from IL-10-/- mice
expressed similar levels of IFN-
, IL-2, and IL-4 after mitogen
stimulation; however, macrophages showed a reduced TNF-
production
compared with IL-10+/- littermates. IL-10-/-
mice had an increased incidence, and a more severe CIA disease than the
IL-10+/- littermates. To study the role of IL-10 in T cell
tolerance, IL-10-/- were crossed into mice carrying the
immunodominant epitope, CII(256–270), in cartilage (MMC) or in skin
(TSC). Both IL-10-/- and IL-10+/- MMC and
TSC mice were completely tolerized against CIA, indicating that lack of
IL-10 in this context did not break tolerance. To investigate whether
IL-10 was important in the effector phase of CIA, arthritis was induced
with anti-CII Abs. Surprisingly, IL-10-/- were less
susceptible to Ab-transferred arthritis, as only 30% showed signs of
disease compared with 90% of the littermates. Therefore, IL-10 seemed
to have a protective role in CIA, but seemed to exacerbate the
arthritogenicity of anti-CII Abs. These data emphasize the
importance of studying IL-10 in a defined genetic context in vivo, to
understand its role in a complex disease like
arthritis.
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