PMID- 9574529
OWN - NLM
STAT- MEDLINE
DCOM- 19980521
LR  - 20171116
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 160
IP  - 9
DP  - 1998 May 1
TI  - Presentation of proteolipid protein epitopes and B7-1-dependent activation of 
      encephalitogenic T cells by IFN-gamma-activated SJL/J astrocytes.
PG  - 4271-9
AB  - There is controversy regarding the possible role of glial cells as APCs in the 
      pathogenesis of central nervous system (CNS) demyelinating diseases such as 
      multiple sclerosis and its animal model, experimental autoimmune 
      encephalomyelitis (EAE). Microglia have been clearly shown to present Ag in the 
      CNS, and due to the proximity of activated astroglial cells to infiltrating T 
      cells and macrophages in demyelinating lesions, it is also possible that 
      astrocytes positively or negatively regulate disease initiation and/or 
      progression. We examined the capacity of IFN-gamma-treated astrocytes from 
      EAE-susceptible SJL/J mice to process and present myelin epitopes. IFN-gamma 
      activation up-regulated ICAM-1, VCAM-1, MHC class II, invariant chain, H2-M, 
      CD40, and B7-1 as determined by FACS and/or RT-PCR analyses. B7-2 expression was 
      only marginally enhanced on SJL/J astrocytes. Consistent with the expression of 
      these accessory molecules, IFN-gamma-treated SJL/J astrocytes induced the 
      B7-1-dependent activation of Th1 lines and lymph node T cells specific for the 
      immunodominant encephalitogenic proteolipid protein (PLP) epitope (PLP139-151) as 
      assessed by proliferation and activation for the adoptive transfer of EAE. 
      Interestingly, IFN-gamma-activated astrocytes efficiently processed and presented 
      PLP139-151, but not the subdominant PLP178-191, PLP56-70, or PLP104-117 epitopes, 
      from intact PLP and a recombinant variant fusion protein of PLP (MP4). The data 
      are consistent with the hypothesis that astrocytes in the proinflammatory CNS 
      environment have the capability of activating CNS-infiltrating encephalitogenic T 
      cells specific for immunodominant epitopes on various myelin proteins that may be 
      involved in either the initial or the relapsing stages of EAE.
FAU - Tan, L
AU  - Tan L
AD  - Department of Microbiology-Immunology and the Interdepartmental Immunobiology 
      Center, Northwestern University Medical School, Chicago, IL 60611, USA.
FAU - Gordon, K B
AU  - Gordon KB
FAU - Mueller, J P
AU  - Mueller JP
FAU - Matis, L A
AU  - Matis LA
FAU - Miller, S D
AU  - Miller SD
LA  - eng
GR  - NS-26543/NS/NINDS NIH HHS/United States
GR  - NS-30871/NS/NINDS NIH HHS/United States
PT  - Journal Article
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 (B7-1 Antigen)
RN  - 0 (Epitopes)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Recombinant Proteins)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Adoptive Transfer
MH  - Animals
MH  - *Antigen Presentation/drug effects
MH  - Astrocytes/drug effects/*immunology
MH  - B7-1 Antigen/*immunology
MH  - Cells, Cultured
MH  - Encephalomyelitis, Autoimmune, Experimental/*immunology
MH  - Epitopes/immunology
MH  - Interferon-gamma/immunology/pharmacology
MH  - Lymphocyte Activation/*immunology
MH  - Mice
MH  - Myelin Sheath/*immunology
MH  - Nerve Tissue Proteins/immunology
MH  - Recombinant Proteins
MH  - T-Lymphocytes/*immunology
EDAT- 1998/05/09 00:00
MHDA- 1998/05/09 00:01
CRDT- 1998/05/09 00:00
PHST- 1998/05/09 00:00 [pubmed]
PHST- 1998/05/09 00:01 [medline]
PHST- 1998/05/09 00:00 [entrez]
PST - ppublish
SO  - J Immunol. 1998 May 1;160(9):4271-9.