{
    "title": "Differential regulation of eosinophil chemokine signaling via CCR3 and non-CCR3 pathways.",
    "journal": "Journal of immunology (Baltimore, Md. : 1950)",
    "date": "1999",
    "authors": "Sabroe I, Hartnell A, Jopling LA, Bel S, Ponath PD, Pease JE, Collins PD, Williams TJ",
    "reference": {
        "type": "PubMed",
        "id": "10072545",
        "url": "https://pubmed.ncbi.nlm.nih.gov/10072545"
    },
    "referenced_proteins": [
        "Q9QXY8-1",
        "D4ABS1-1",
        "Q5PPP2-1",
        "O00175-1"
    ],
    "referenced_glycans": [],
    "species": [
        {
            "name": "Rattus norvegicus",
            "taxid": 10116,
            "evidence": [
                {
                    "database": "UniProtKB",
                    "id": "Q9QXY8",
                    "url": "https://www.uniprot.org/uniprot/Q9QXY8"
                }
            ],
            "common_name": "Rat"
        }
    ],
    "record_id": "pubmed.10072545",
    "abstract": "To investigate eosinophil stimulation by chemokines we developed a sensitive assay of leukocyte shape change, the gated autofluorescence/forward scatter assay. Leukocyte shape change responses are mediated through rearrangements of the cellular cytoskeleton in a dynamic process typically resulting in a polarized cell and are essential to the processes of leukocyte migration from the microcirculation into sites of inflammation. We examined the actions of the chemokines eotaxin, eotaxin-2, monocyte chemoattractant protein-1 (MCP-1), MCP-3, MCP-4, RANTES, macrophage inflammatory protein-1alpha (MIP-1alpha), and IL-8 on leukocytes in mixed cell suspensions and focused on the responses of eosinophils to C-C chemokines. Those chemokines acting on CCR3 induced a rapid shape change in eosinophils from all donors; of these, eotaxin and eotaxin-2 were the most potent. Responses to MCP-4 were qualitatively different, showing marked reversal of shape change responses with agonist concentration and duration of treatment. In contrast, MIP-1alpha induced a potent response in eosinophils from a small and previously undescribed subgroup of donors via a non-CCR3 pathway likely to be CCR1 mediated. Incubation of leukocytes at 37 degrees C for 90 min in the absence of extracellular calcium up-regulated responses to MCP-4 and MIP-1alpha in the majority of donors, and there was a small increase in responses to eotaxin. MIP-1alpha responsiveness in vivo may therefore be a function of both CCR1 expression levels and the regulated efficiency of coupling to intracellular signaling pathways. The observed up-regulation of MIP-1alpha signaling via non-CCR3 pathways may play a role in eosinophil recruitment in inflammatory states such as occurs in the asthmatic lung.",
    "glycosylation": [],
    "mutagenesis": [],
    "snv": [],
    "phosphorylation": [],
    "glycation": []
}