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Ann Rheum Dis doi:10.1136/ard.2007.076976

Cellular distribution of the C-type II lectin DCIR and its expression in the rheumatic joint- identification of a subpopulation of DCIR+ T cells

  1. Carina Eklöw (carina.eklow{at}ki.se)
  1. Karolinska Institutet, Sweden
    1. Dimitrios Makrygiannakis
    1. Karolinska Institutet, Sweden
      1. Liselotte Bäckdahl
      1. Karolinska Institutet, Sweden
        1. Leonid Padyukov
        1. Karolinska Institutet, Sweden
          1. Ann-Kristin Ulfgren
          1. Karolinska Institutet, Sweden
            1. Johnny C Lorentzen
            1. Karolinska Institutet, Sweden
              1. Vivianne Malmström (vivianne.malmstrom{at}ki.se)
              1. Karolinska Institutet, Sweden
                • Published Online First 4 February 2008

                Abstract

                Objective: An association to variations in the dendritic cell immunoreceptor (DCIR) gene with rheumatoid arthritis (RA) was recently shown. However, protein expression of DCIR has so far not been assessed in a disease setting. Here, we aimed to determine the cellular and tissue distribution of this receptor in healthy controls and in RA patients before and after local glucocorticoid administration.

                Methods: DCIR mRNA expression was evaluated by quantitative PCR (n=3) and protein expression by flow cytometry (n=18), immunohistochemistry (n=14) and double immunofluorescence (n=5).

                Results: DCIR protein was not detected in healthy synovia. In contrast, expression was abundant on cells from rheumatic joints, both in synovial fluid and tissue. Following corticosteroid treatment this expression was down regulated. Interestingly, DCIR could be detected on NK-cells and T-cells, both CD4+ and CD8+, as well as on monocytes, B-cells, dendritic cells and granulocytes. Both the frequency of DCIR+ T-cells and the level of surface expression was increased in the rheumatic joint compared to blood. In synovial fluid the typical DCIR+ T-cells were large activated cells, whereas blasted DCIR+ T-cells were not detected in blood.

                Conclusions: We demonstrate increased protein and mRNA expression of DCIR in RA, especially in the rheumatic joint. Expression was wide spread and included a subpopulation of T-cells. This suggests that the inflammatory synovial environment induces DCIR expression, and this may be related to synovial T-cell function. Ligation of DCIR, or lack thereof, could contribute to the chronic inflammation characterizing autoimmune diseases such as RA.

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