Abstract

Abstract The DA rat is a commonly used inbred rat strain in inflammation research due to its susceptibility to numerous experimentally induced models of autoimmunity. We have isolated a spontaneous mutation that abrogates induction of a panel of inflammatory disorders in the DA rat and mapped it to a 2,5Mb region on chromosome 9. This new subset of the DA rat was called DA completely protected, DACP. To elucidate if the protection seen in the DACP rat is conveyed during the induction or the effector phase we utilized the Pristane-induced arthritis transfer model in a reciprocal fashion. Our results showed that cells from the DACP rat did not transfer arthritis to susceptible DA rats whereas cells from the susceptible DA rat caused a mild arthritis in DACP recipients. Looking at the cytokine profile of these cells we saw that cells from the DACP rat produced twice the amount of IL-10 compared to cells from the DA rat and that the production of RANTES was lower in the DACP rat. Differences in levels of IL-10 and RANTES could be one possible explanation for the protection seen in the DACP rat however this remains to be shown. In summary, the DACP rat was unable to develop disease upon arthritis induction but could develop a mild arthritis when receiving arthritogenic cells from the DA rat. Our findings suggest a possible dual role of the spontaneous mutation in the induction phase and the effector phase of arthritis in the DACP rat.

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