| First Author | Robben PM | Year | 2005 |
| Journal | J Exp Med | Volume | 201 |
| Issue | 11 | Pages | 1761-9 |
| PubMed ID | 15928200 | Mgi Jnum | J:99209 |
| Mgi Id | MGI:3581479 | Doi | 10.1084/jem.20050054 |
| Citation | Robben PM, et al. (2005) Recruitment of Gr-1+ monocytes is essential for control of acute toxoplasmosis. J Exp Med 201(11):1761-9 |
| abstractText | Circulating murine monocytes comprise two largely exclusive subpopulations that are responsible for seeding normal tissues (Gr-1(-)/CCR2(-)/CX(3)CR1(high)) or responding to sites of inflammation (Gr-1(+)/CCR2(+)/CX(3)CR1(lo)). Gr-1(+) monocytes are recruited to the site of infection during the early stages of immune response to the intracellular pathogen Toxoplasma gondii. A murine model of toxoplasmosis was thus used to examine the importance of Gr-1(+) monocytes in the control of disseminated parasitic infection in vivo. The recruitment of Gr-1(+) monocytes was intimately associated with the ability to suppress early parasite replication at the site of inoculation. Infection of CCR2(-/-) and MCP-1(-/-) mice with typically nonlethal, low doses of T. gondii resulted in the abrogated recruitment of Gr-1(+) monocytes. The failure to recruit Gr-1(+) monocytes resulted in greatly enhanced mortality despite the induction of normal Th1 cell responses leading to high levels of IL-12, TNF-alpha, and IFN-gamma. The profound susceptibility of CCR2(-/-) mice establishes Gr-1(+) monocytes as necessary effector cells in the resistance to acute toxoplasmosis and suggests that the CCR2-dependent recruitment of Gr-1(+) monocytes may be an important general mechanism for resistance to intracellular pathogens. |
