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The atypical chemokine receptor ACKR2 is expressed by lymphatic endothelial cells and scavenges pro\u2010inflammatory CC chemokines to indirectly subdue leukocyte migration. This contributes to the resolution of acute inflammatory responses <jats:italic>in vivo<\/jats:italic>. ACKR2 is also universally expressed by innate\u2010like B cells, suppressing their responsiveness to the non\u2010ACKR2 ligand CXCL13, and controlling their distribution <jats:italic>in vivo<\/jats:italic>. The role of ACKR2 in autoimmunity remains relatively unexplored, although <jats:italic>Ackr2<\/jats:italic> deficiency reportedly lessens the clinical symptoms of experimental autoimmune encephalomyelitis induced by immunization with encephalogenic peptide (MOG<jats:sub>35\u201355<\/jats:sub>). This was attributed to poor T\u2010cell priming stemming from the defective departure of dendritic cells from the site of immunization. However, we report here that <jats:italic>Ackr2<\/jats:italic>\u2010deficient mice, on two separate genetic backgrounds, are not less susceptible to autoimmunity induced by immunization, and in some cases develop enhanced clinical symptoms. Moreover, ACKR2 deficiency does not suppress T\u2010cell priming in response to encephalogenic peptide (MOG<jats:sub>35\u201355<\/jats:sub>), and responses to protein antigen (collagen or MOG<jats:sub>1\u2013125<\/jats:sub>) are characterized by elevated interleukin\u201017 production. Interestingly, after immunization with protein, but not peptide, antigen, <jats:italic>Ackr2<\/jats:italic> deficiency was also associated with an increase in lymph node B cells expressing granulocyte\u2010macrophage colony\u2010stimulating factor (GM\u2010CSF), a cytokine that enhances T helper type 17 (Th17) cell development and survival. Thus, <jats:italic>Ackr2<\/jats:italic> deficiency does not suppress autoreactive T\u2010cell priming and autoimmune pathology, but can enhance T\u2010cell polarization toward Th17 cells and increase the abundance of GM\u2010CSF<jats:sup>+<\/jats:sup> B cells in lymph nodes draining the site of immunization.<\/jats:p>","DOI":"10.1038\/icb.2014.90","type":"journal-article","created":{"date-parts":[[2014,10,28]],"date-time":"2014-10-28T10:44:43Z","timestamp":1414493083000},"page":"167-176","source":"Crossref","is-referenced-by-count":21,"title":["The atypical chemokine receptor ACKR2 suppresses Th17 responses to protein autoantigens"],"prefix":"10.1111","volume":"93","author":[{"given":"Chris AH","family":"Hansell","sequence":"first","affiliation":[{"name":"Institute of Infection, Immunity and Inflammation, College of Medical Veterinary and Life Sciences, University of Glasgow Glasgow UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lindsay 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