PMID- 10605038
OWN - NLM
STAT- MEDLINE
DCOM- 20000119
LR  - 20190515
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 164
IP  - 1
DP  - 2000 Jan 1
TI  - Kinetics and cellular origin of cytokines in the central nervous system: insight 
      into mechanisms of myelin oligodendrocyte glycoprotein-induced experimental 
      autoimmune encephalomyelitis.
PG  - 419-26
AB  - Experimental autoimmune encephalomyelitis induced by myelin oligodendrocyte 
      glycoprotein (MOG) in C57BL/6 (H-2b) mice is characterized by early (day 12) 
      acute paralysis, followed by a sustained chronic clinical course that gradually 
      stabilizes. Extensive inflammation and demyelination coincide with clinical signs 
      of disease. To identify the mechanisms of these processes, individual 
      proinflammatory and anti-inflammatory cytokines and chemokines were studied. 
      Sensitive single-cell assays were utilized to determine the cellular origin and 
      kinetics of cytokine production in the CNS. Immunization with MOG35-55 peptide 
      resulted in priming of both Th1 (lymphotoxin, IFN-gamma, and TNF-alpha) and Th2 
      (IL-4) cells in the spleen. However, only Th1 cells were apparent in the CNS. CD4 
      T cells that produced IFN-gamma or TNF-alpha were present in the CNS by day 7 
      after immunization with MOG35-55, peaked at day 20, and then waned. TNF-alpha was 
      also produced in the CNS by Mac-1+ cells. On days 7 and 10 after immunization, 
      the TNF-alpha-producing Mac1+ cells were predominantly microglia. By day 14, a 
      switch occurred in that the Mac1+ TNF-alpha-producing cells had the phenotype of 
      infiltrating macrophages. RANTES, IFN-inducible protein 10 (IP-10), and monocyte 
      chemotactic protein 1 chemokine mRNA were detected in the CNS by day 8 after 
      immunization. The early presence of monocyte chemotactic protein 1 (MCP-1) in the 
      CNS provides a mechanism for the recruitment of macrophages. These data implicate 
      TNF-alpha production by a continuum of T cells, microglia, and macrophages at 
      various times during the course of disease. The importance of Th1 cytokines is 
      highlighted, with little evidence for a role of Th2 cytokines.
FAU - Juedes, A E
AU  - Juedes AE
AD  - Department of Epidemiology and Public Health, Section of Immunobiology, Yale 
      University School of Medicine, New Haven, CT 06520, USA.
FAU - Hjelmstrom, P
AU  - Hjelmstrom P
FAU - Bergman, C M
AU  - Bergman CM
FAU - Neild, A L
AU  - Neild AL
FAU - Ruddle, N H
AU  - Ruddle NH
LA  - eng
GR  - TG AI 07019/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Mog protein, mouse)
RN  - 0 (Myelin Proteins)
RN  - 0 (Myelin-Associated Glycoprotein)
RN  - 0 (Myelin-Oligodendrocyte Glycoprotein)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Central Nervous System/cytology/*immunology/*metabolism
MH  - Chemokines/biosynthesis
MH  - Cytokines/*biosynthesis
MH  - Encephalomyelitis, Autoimmune, Experimental/etiology/*immunology/metabolism
MH  - Female
MH  - Immunophenotyping
MH  - Inflammation Mediators/metabolism
MH  - Injections, Subcutaneous
MH  - Interferon-gamma/biosynthesis/metabolism
MH  - Kinetics
MH  - Lymphocyte Activation
MH  - Macrophages/immunology/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Microglia/immunology/metabolism
MH  - Molecular Sequence Data
MH  - Myelin Proteins
MH  - Myelin-Associated Glycoprotein/administration & dosage/*immunology
MH  - Myelin-Oligodendrocyte Glycoprotein
MH  - Spleen/cytology/immunology/metabolism
MH  - Th1 Cells/immunology/metabolism
MH  - Th2 Cells/immunology/metabolism
MH  - Tumor Necrosis Factor-alpha/biosynthesis/metabolism
EDAT- 1999/12/22 00:00
MHDA- 1999/12/22 00:01
CRDT- 1999/12/22 00:00
PHST- 1999/12/22 00:00 [pubmed]
PHST- 1999/12/22 00:01 [medline]
PHST- 1999/12/22 00:00 [entrez]
AID - ji_v164n1p419 [pii]
AID - 10.4049/jimmunol.164.1.419 [doi]
PST - ppublish
SO  - J Immunol. 2000 Jan 1;164(1):419-26. doi: 10.4049/jimmunol.164.1.419.