Control of TH2 polarization by the chemokine monocyte chemoattractant protein-1

Long Gu, Susan Tseng, Renée M. Horner, Carmen Tam, Massimo Loda and Barrett J. Rollins ()
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Long Gu: Dana-Farber Cancer Institute, Brigham & Women's Hospital, and Harvard Medical School
Susan Tseng: Dana-Farber Cancer Institute, Brigham & Women's Hospital, and Harvard Medical School
Renée M. Horner: Dana-Farber Cancer Institute, Brigham & Women's Hospital, and Harvard Medical School
Carmen Tam: Dana-Farber Cancer Institute, Brigham & Women's Hospital, and Harvard Medical School
Massimo Loda: Dana-Farber Cancer Institute, Brigham & Women's Hospital, and Harvard Medical School
Barrett J. Rollins: Dana-Farber Cancer Institute, Brigham & Women's Hospital, and Harvard Medical School

Nature, 2000, vol. 404, issue 6776, 407-411

Abstract: Abstract Activated T lymphocytes differentiate into effector cells tailored to meet disparate challenges to host integrity1. For example, type 1 and type 2 helper (TH1 and TH2) cells secrete cytokines that enhance cell-mediated and humoral immunity, respectively. The chemokine monocyte chemoattractant protein-1 (MCP-1) can stimulate interleukin-4 production2 and its overexpression is associated with defects in cell-mediated immunity3, indicating that it might be involved in TH2 polarization. Here we show that MCP-1-deficient mice are unable to mount TH2 responses. Lymph node cells from immunized MCP-1-/- mice synthesize extremely low levels of interleukin-4, interleukin-5 and interleukin-10, but normal amounts of interferon-γ and interleukin-2. Consequently, these mice do not accomplish the immunoglobulin subclass switch that is characteristic of TH2 responses and are resistant to Leishmania major. These effects are direct rather than due to abnormal cell migration, because the trafficking of naive T cells is undisturbed in MCP-1-/- mice despite the presence of MCP-1-expressing cells in secondary lymphoid organs of wild-type mice. Thus, MCP-1 influences both innate immunity, through effects on monocytes, and adaptive immunity, through control of T helper cell polarization.

Date: 2000
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DOI: 10.1038/35006097

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