PMID- 7511974
OWN - NLM
STAT- MEDLINE
DCOM- 19940509
LR  - 20190512
IS  - 0006-8950 (Print)
IS  - 0006-8950 (Linking)
VI  - 117 ( Pt 1)
DP  - 1994 Feb
TI  - Human astrocytes are only partially competent antigen presenting cells. Possible 
      implications for lesion development in multiple sclerosis.
PG  - 59-69
AB  - Highly purified astrocyte cultures from human embryonic brain were examined for 
      their capacity to present antigen to human leukocyte antigen (HLA) class II 
      compatible, cytolytic CD4+ T lymphocytes. Most astrocytes constitutively 
      expressed HLA class I products and LFA-3 (CD58). Constitutive expression of HLA 
      class II, LFA-1 alpha (CD11a) and ICAM-1 (CD54) was lower and varied among 
      different cultures, while LFA-2 (CD2) was absent. IFN-gamma alone or in 
      combination with TNF-alpha strongly enhanced expression of HLA class I, HLA-DR, 
      -DP, -DQ, LFA-1 alpha and ICAM-1, but did not affect expression of LFA-2 (CD2) 
      and LFA-3 (CD58). TNF-alpha alone induced only HLA class I and ICAM-1, but not 
      HLA class II or LFA-1 alpha. Cytokine treated, but not untreated astrocytes were 
      able to present protein (auto-)antigens to specific T lymphocyte lines. 
      Astrocytes expressing appropriate major histocompatibility complex class II 
      products were lysed by CD4+ T cells specific for myelin basic protein or tetanus 
      toxoid. The lytic response was antigen dose dependent and HLA-DR restricted. It 
      could be blocked by antibodies against HLA-DR determinants and against the 
      adhesion molecules LFA-1 alpha and ICAM-1. In remarkable contrast to their 
      susceptibility to T cell lysis, antigen presenting astrocytes were not only 
      completely unable to induce T cell proliferation but even inhibited 
      proliferation. The results indicate that, although human astrocytes have the 
      potential to present protein antigens to CD4+ T cells, they do not induce the 
      co-stimulatory factors required to trigger the complete T cell activation 
      programme.
FAU - Weber, F
AU  - Weber F
AD  - Department of Neuroimmunology, Max-Planck-Institute of Psychiatry, Martinsried, 
      Germany.
FAU - Meinl, E
AU  - Meinl E
FAU - Aloisi, F
AU  - Aloisi F
FAU - Nevinny-Stickel, C
AU  - Nevinny-Stickel C
FAU - Albert, E
AU  - Albert E
FAU - Wekerle, H
AU  - Wekerle H
FAU - Hohlfeld, R
AU  - Hohlfeld R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Brain
JT  - Brain : a journal of neurology
JID - 0372537
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, Differentiation, T-Lymphocyte)
RN  - 0 (CD2 Antigens)
RN  - 0 (CD58 Antigens)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Epitopes)
RN  - 0 (HLA Antigens)
RN  - 0 (Lymphocyte Function-Associated Antigen-1)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Antigen-Presenting Cells/*immunology
MH  - Antigens, CD/immunology
MH  - Antigens, Differentiation, T-Lymphocyte/immunology
MH  - Astrocytes/*immunology
MH  - CD2 Antigens
MH  - CD58 Antigens
MH  - Cell Adhesion Molecules/immunology
MH  - Cell Division
MH  - Cell Line
MH  - Epitopes
MH  - HLA Antigens/*immunology
MH  - Humans
MH  - Intercellular Adhesion Molecule-1
MH  - Interferon-gamma/immunology
MH  - Lymphocyte Function-Associated Antigen-1/immunology
MH  - Membrane Glycoproteins/immunology
MH  - Multiple Sclerosis/*immunology
MH  - Receptors, Immunologic/immunology
MH  - T-Lymphocytes/cytology/immunology
MH  - Tumor Necrosis Factor-alpha/immunology
EDAT- 1994/02/01 00:00
MHDA- 1994/02/01 00:01
CRDT- 1994/02/01 00:00
PHST- 1994/02/01 00:00 [pubmed]
PHST- 1994/02/01 00:01 [medline]
PHST- 1994/02/01 00:00 [entrez]
AID - 10.1093/brain/117.1.59 [doi]
PST - ppublish
SO  - Brain. 1994 Feb;117 ( Pt 1):59-69. doi: 10.1093/brain/117.1.59.