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Although\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      infection elicits a protective immune response, the nature of the monocyte response in the immediate vicinity of parasites during initial brain infection is not well understood. By infecting mice with\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      and comparing areas of the brain containing or not containing parasites, we found an increase in CCR2\n                      <jats:sup>+<\/jats:sup>\n                      monocytes, IBA1\n                      <jats:sup>+<\/jats:sup>\n                      myeloid cells, GFAP\n                      <jats:sup>+<\/jats:sup>\n                      astrocytes, and CD68\n                      <jats:sup>+<\/jats:sup>\n                      signal near parasites in the brain, indicating immune cell infiltration and phagolysosomal activation in response to the infection. CCR2\n                      <jats:sup>+<\/jats:sup>\n                      CD68\n                      <jats:sup>+<\/jats:sup>\n                      monocytes were specifically increased near tachyzoites with minimal localization of these cells near cysts in the brain. This monocyte response was also detected near parasite-interacted cells, identified using\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      parasites that inject Cre recombinase into \u201cinteracted\u201d cells of Ai6 CCR2\n                      <jats:sup>RFP\/+<\/jats:sup>\n                      mice, enabling us to track these events\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      . The chemokine CCL2 and its transcription factor NF-\u03baB were also upregulated surrounding parasites in the brain; however, the\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      effector protein GRA15, which sustains NF-\u03baB activation in infected cells, was not required for CCL2 production, NF-\u03baB activation, or myeloid cell recruitment to parasites in the brain. In contrast, active\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      replication played a more significant role, as CCR2\n                      <jats:sup>+<\/jats:sup>\n                      monocytes were recruited to replication-competent but not replication-deficient\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      delivered via intracranial injection into mice. These findings provide novel insights into the drivers of immune cell mobilization and activation in the brain during initial\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      central nervous system infection and highlight the importance of parasite replication in this process.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Toxoplasma gondii<\/jats:italic>\n                      is a brain-infecting parasite, and the mobilization of peripheral immune cells to the brain is critical for controlling\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      infection. However, the initial events driving these cells to sites of\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      infection in the brain are poorly understood. We show that peripheral myeloid immune cell recruitment and activation are specific to areas of the brain containing actively replicating parasites, which are capable of lysing host cells. This local immune response is characterized by focal chemokine production, myeloid cell recruitment, and the activation of phagolysosomal pathways. These highly localized host responses were independent of the parasite effector protein that induces NF-\u03baB activation within infected cells, GRA15. However, the localized monocyte recruitment was dependent on live parasites and active parasite replication. This research highlights the importance of host cell sensing of parasite replication in the brain for immune control of\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      infection.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.00810-25","type":"journal-article","created":{"date-parts":[[2025,6,10]],"date-time":"2025-06-10T09:00:31Z","timestamp":1749546031000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":5,"title":["<i>Toxoplasma gondii<\/i>\n                    parasites induce a localized myeloid cell immune response surrounding parasites in the brain during acute infection"],"prefix":"10.1128","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2491-1074","authenticated-orcid":true,"given":"Stephanie 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