PMID- 11106572
OWN - NLM
STAT- MEDLINE
DCOM- 20010104
LR  - 20181113
IS  - 0002-9440 (Print)
IS  - 1525-2191 (Electronic)
IS  - 0002-9440 (Linking)
VI  - 157
IP  - 6
DP  - 2000 Dec
TI  - Intracerebral recruitment and maturation of dendritic cells in the onset and 
      progression of experimental autoimmune encephalomyelitis.
PG  - 1991-2002
AB  - Dendritic cells (DCs) are thought to be key elements in the initiation and 
      maintenance of autoimmune diseases. In this study, we sought evidence that DCs 
      recruited to the central nervous system (CNS), a site that is primarily devoid of 
      resident DCs, play a role in the effector phase and propagation of the immune 
      response in experimental autoimmune encephalomyelitis (EAE). After immunization 
      of SJL mice with proteolipid protein 139-151 peptide, process-bearing cells 
      expressing the DC markers DEC-205 and CD11c appeared early in the spinal cord. 
      During acute, chronic, and relapsing EAE, DEC-205(+) DCs expressing a 
      lymphostimulatory phenotype (including the mature DC marker MIDC-8, major 
      histocompatibility complex class II, CD40, and CD86 molecules) accumulated within 
      the CNS inflammatory cell infiltrates. More prominent infiltration of the spinal 
      cord parenchyma by mature DCs was observed in mice with relapsing disease. 
      Macrophage inflammatory protein 3alpha, a chemokine active on DCs and 
      lymphocytes, and its receptor CCR6 were up-regulated in the CNS during EAE. These 
      findings suggest that intracerebral recruitment and maturation of DCs may be 
      crucial in the local stimulation and maintenance of autoreactive immune 
      responses, and that therapeutic strategies aimed at manipulating DC migration 
      could be useful in the treatment of CNS autoimmune disorders.
FAU - Serafini, B
AU  - Serafini B
AD  - Laboratory of Organ and System Pathophysiology, Istituto Superiore di Sanita, 
      Rome, Italy.
FAU - Columba-Cabezas, S
AU  - Columba-Cabezas S
FAU - Di Rosa, F
AU  - Di Rosa F
FAU - Aloisi, F
AU  - Aloisi F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Pathol
JT  - The American journal of pathology
JID - 0370502
RN  - 0 (CCL20 protein, human)
RN  - 0 (CCR6 protein, human)
RN  - 0 (Chemokine CCL20)
RN  - 0 (Chemokines, CC)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Receptors, CCR6)
RN  - 0 (Receptors, Chemokine)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Cellular Senescence
MH  - Central Nervous System/metabolism/pathology/*physiopathology
MH  - Chemokine CCL20
MH  - *Chemokines, CC
MH  - Choroid Plexus/pathology
MH  - Chronic Disease
MH  - Dendritic Cells/immunology/*physiology
MH  - Disease Progression
MH  - Encephalomyelitis, Autoimmune, Experimental/*immunology/pathology/physiopathology
MH  - Female
MH  - Macrophage Inflammatory Proteins/metabolism
MH  - Meninges/pathology
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Receptors, CCR6
MH  - Receptors, Chemokine/metabolism
MH  - Recurrence
MH  - Spinal Cord/pathology
MH  - Time Factors
MH  - Up-Regulation
PMC - PMC1885753
EDAT- 2000/12/07 11:00
MHDA- 2001/02/28 10:01
PMCR- 2001/06/01
CRDT- 2000/12/07 11:00
PHST- 2000/12/07 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/12/07 11:00 [entrez]
PHST- 2001/06/01 00:00 [pmc-release]
AID - S0002-9440(10)64838-9 [pii]
AID - 2413 [pii]
AID - 10.1016/S0002-9440(10)64838-9 [doi]
PST - ppublish
SO  - Am J Pathol. 2000 Dec;157(6):1991-2002. doi: 10.1016/S0002-9440(10)64838-9.