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Background  Spondyloarthritis (SpA) is a chronic inflammatory disease affecting primarily axial and peripheral joints and sometimes also extra-articular organs, such as the gut. Rats transgenic for HLA-B27 and human β2-microglobulin (B27-Tg rat) develop clinical manifestations resembling human disease. In this model, it has been shown that CD103 +  conventional dendritic cells (cDCs) exhibited altered functions, likely promoting SpA development. CD4 −  cDC subpopulation expressing XCR1, a chemokine receptor involved in their migration, have been described to be tolerogenic in steady state. Thus, in this study, we wished to examine the fate of XCR1 +  cDCs in this animal model of SpA.    Methods  cDC populations were isolated from the spleen, mesenteric lymph nodes (MLN), and colonic  lamina propria  from B27-TG and control nontransgenic (NTG) and/or HLA-B7 transgenic rats after collagenase digestion and density gradient and characterized with flow cytometry or real-time PCR. Migration of cDCs from intestinal mucosa to MLN was assessed, using TLR-7 stimulation with Resiquimod.    Results  We observed a reduced frequency of cCD4 −  DCs in B27-Tg rats, as compared to control rats. Furthermore, such decrease was not due to excessive death of CD4 −  cDCs in B27-Tg rats. Interestingly, we observed a decrease frequency of the XCR1 +  subpopulation among CD4 −  cDCs in the spleen, MLN, and  lamina propria  from B27-Tg rats. Finally, after TLR-7 stimulation, the migration of XCR1 +  cDCs to MLN was proportionally reduced in B27-Tg rats.    Conclusion  Our results demonstrate for the first time a decreased proportion of the tolerogenic XCR1 +  cDC subpopulation in SpA target organs in B27-Tg rat, which may affect the maintenance of self-tolerance and control of inflammation.    Electronic supplementary material  The online version of this article (10.1186/s13075-019-1827-9) contains supplementary material, which is available to authorized users.

Tolerogenic XCR1+ dendritic cell population is dysregulated in HLA-B27 transgenic rat model of spondyloarthritis