PMID- 10746730
OWN - NLM
STAT- MEDLINE
DCOM- 20000413
LR  - 20220311
IS  - 0028-0836 (Print)
IS  - 0028-0836 (Linking)
VI  - 404
IP  - 6776
DP  - 2000 Mar 23
TI  - Control of TH2 polarization by the chemokine monocyte chemoattractant protein-1.
PG  - 407-11
AB  - Activated T lymphocytes differentiate into effector cells tailored to meet 
      disparate challenges to host integrity. For example, type 1 and type 2 helper 
      (T(H)1 and T(H)2) cells secrete cytokines that enhance cell-mediated and humoral 
      immunity, respectively. The chemokine monocyte chemoattractant protein-1 (MCP-1) 
      can stimulate interleukin-4 production and its overexpression is associated with 
      defects in cell-mediated immunity, indicating that it might be involved in T(H)2 
      polarization. Here we show that MCP-1-deficient mice are unable to mount T(H)2 
      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-gamma and interleukin-2. Consequently, these mice do not accomplish 
      the immunoglobulin subclass switch that is characteristic of T(H)2 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.
FAU - Gu, L
AU  - Gu L
AD  - Department of Adult Oncology, Dana-Farber Cancer Institute, Brigham & Women's 
      Hospital, and Harvard Medical School, Boston, Massachusetts 02115, USA.
FAU - Tseng, S
AU  - Tseng S
FAU - Horner, R M
AU  - Horner RM
FAU - Tam, C
AU  - Tam C
FAU - Loda, M
AU  - Loda M
FAU - Rollins, B J
AU  - Rollins BJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Nature
JT  - Nature
JID - 0410462
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Immunoglobulin G)
RN  - 207137-56-2 (Interleukin-4)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/deficiency/*physiology
MH  - Cytokines/biosynthesis
MH  - Immunity
MH  - Immunoglobulin G/immunology
MH  - Interleukin-4/biosynthesis
MH  - Leishmania major/immunology
MH  - Lymph Nodes/immunology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Spleen/immunology
MH  - Th2 Cells/*immunology
EDAT- 2000/04/04 09:00
MHDA- 2000/04/15 09:00
CRDT- 2000/04/04 09:00
PHST- 1999/12/20 00:00 [received]
PHST- 2000/01/26 00:00 [accepted]
PHST- 2000/04/04 09:00 [pubmed]
PHST- 2000/04/15 09:00 [medline]
PHST- 2000/04/04 09:00 [entrez]
AID - 35006097 [pii]
AID - 10.1038/35006097 [doi]
PST - ppublish
SO  - Nature. 2000 Mar 23;404(6776):407-11. doi: 10.1038/35006097.