Abstract
Murine retinal glia are normally negative for major histocompatibility complex (MHC) Class II antigens and express low levels of MHC Class I and intercellular adhesion molecule-1 (ICAM-1) as detected by avidin-biotin-peroxidase immunohistochemistry. These surface molecules associated with immune function were either induced (Class II) or upregulated (Class I and ICAM-1) on cultured retinal glial cells in a dose- and time-dependent manner following exposure to recombinant interferon-γ (rlFN-γ). MHC Class I and II expression by passaged and primary cells was maximal (> 90% positive) after incubation with 100 U/ml of rIFN-γ for 48 h. ICAM-1 expression by primary and passaged cells tripled between 48 and 72 h after exposure to 25 or 50 U/ml of rIFN-γ. By 72 h after exposure to 100 U/ml of rIFN-γ, 62% of the retinal glia were positive for ICAM-1, whereas under normal culture conditions these molecules were detected on <3% of the retinal glia. Bacterial lipopolysaccharide (LPS), a known stimulator of central nervous system (CNS) astrocytes, increased ICAM-1 expression only 3-fold to 9% of cells staining positively, but neither MHC Class I nor Class II expression was altered from baseline levels. Surface expression of ICAM-I, MHC Class I, and MHC Class II was unaffected by exposure to either rTNF-α (1000 U/ml) or rIL-6 (100 U/ml) for 24 h. Under normal culture conditions, intracellular interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected immunohistochemically. Exposure to either rIFN-γ or LPS induced more intense staining which correlated with increased secreted levels of both cytokines in culture supernatants. Levels of secreted TNF-α increased 6-fold after stimulation with LPS for 24 h, while secreted IL-6 increased over 9-fold. These results support the hypothesis that retinal glia may participate in intraretinal immune processes following stimulation during inflammatory and infectious processes via either cell surface- or soluble mediator-dependent mechanisms or a combination of both.
| Original language | English |
|---|---|
| Pages (from-to) | 71-81 |
| Number of pages | 11 |
| Journal | Journal of Neuroimmunology |
| Volume | 64 |
| Issue number | 1 |
| DOIs | |
| State | Published - 1996 |
| Externally published | Yes |
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All Science Journal Classification (ASJC) codes
- Immunology
- Clinical Neurology
- Immunology and Allergy
- Neurology
Cite this
Modulation of immune-associated surface markers and cytokine production by murine retinal glial cells. / Drescher, Kristen M.; Whittum-Hudson, Judith A.
In: Journal of Neuroimmunology, Vol. 64, No. 1, 1996, p. 71-81.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Modulation of immune-associated surface markers and cytokine production by murine retinal glial cells
AU - Drescher, Kristen M.
AU - Whittum-Hudson, Judith A.
PY - 1996
Y1 - 1996
N2 - Murine retinal glia are normally negative for major histocompatibility complex (MHC) Class II antigens and express low levels of MHC Class I and intercellular adhesion molecule-1 (ICAM-1) as detected by avidin-biotin-peroxidase immunohistochemistry. These surface molecules associated with immune function were either induced (Class II) or upregulated (Class I and ICAM-1) on cultured retinal glial cells in a dose- and time-dependent manner following exposure to recombinant interferon-γ (rlFN-γ). MHC Class I and II expression by passaged and primary cells was maximal (> 90% positive) after incubation with 100 U/ml of rIFN-γ for 48 h. ICAM-1 expression by primary and passaged cells tripled between 48 and 72 h after exposure to 25 or 50 U/ml of rIFN-γ. By 72 h after exposure to 100 U/ml of rIFN-γ, 62% of the retinal glia were positive for ICAM-1, whereas under normal culture conditions these molecules were detected on <3% of the retinal glia. Bacterial lipopolysaccharide (LPS), a known stimulator of central nervous system (CNS) astrocytes, increased ICAM-1 expression only 3-fold to 9% of cells staining positively, but neither MHC Class I nor Class II expression was altered from baseline levels. Surface expression of ICAM-I, MHC Class I, and MHC Class II was unaffected by exposure to either rTNF-α (1000 U/ml) or rIL-6 (100 U/ml) for 24 h. Under normal culture conditions, intracellular interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected immunohistochemically. Exposure to either rIFN-γ or LPS induced more intense staining which correlated with increased secreted levels of both cytokines in culture supernatants. Levels of secreted TNF-α increased 6-fold after stimulation with LPS for 24 h, while secreted IL-6 increased over 9-fold. These results support the hypothesis that retinal glia may participate in intraretinal immune processes following stimulation during inflammatory and infectious processes via either cell surface- or soluble mediator-dependent mechanisms or a combination of both.
AB - Murine retinal glia are normally negative for major histocompatibility complex (MHC) Class II antigens and express low levels of MHC Class I and intercellular adhesion molecule-1 (ICAM-1) as detected by avidin-biotin-peroxidase immunohistochemistry. These surface molecules associated with immune function were either induced (Class II) or upregulated (Class I and ICAM-1) on cultured retinal glial cells in a dose- and time-dependent manner following exposure to recombinant interferon-γ (rlFN-γ). MHC Class I and II expression by passaged and primary cells was maximal (> 90% positive) after incubation with 100 U/ml of rIFN-γ for 48 h. ICAM-1 expression by primary and passaged cells tripled between 48 and 72 h after exposure to 25 or 50 U/ml of rIFN-γ. By 72 h after exposure to 100 U/ml of rIFN-γ, 62% of the retinal glia were positive for ICAM-1, whereas under normal culture conditions these molecules were detected on <3% of the retinal glia. Bacterial lipopolysaccharide (LPS), a known stimulator of central nervous system (CNS) astrocytes, increased ICAM-1 expression only 3-fold to 9% of cells staining positively, but neither MHC Class I nor Class II expression was altered from baseline levels. Surface expression of ICAM-I, MHC Class I, and MHC Class II was unaffected by exposure to either rTNF-α (1000 U/ml) or rIL-6 (100 U/ml) for 24 h. Under normal culture conditions, intracellular interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected immunohistochemically. Exposure to either rIFN-γ or LPS induced more intense staining which correlated with increased secreted levels of both cytokines in culture supernatants. Levels of secreted TNF-α increased 6-fold after stimulation with LPS for 24 h, while secreted IL-6 increased over 9-fold. These results support the hypothesis that retinal glia may participate in intraretinal immune processes following stimulation during inflammatory and infectious processes via either cell surface- or soluble mediator-dependent mechanisms or a combination of both.
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U2 - 10.1016/0165-5728(95)00156-5
DO - 10.1016/0165-5728(95)00156-5
M3 - Article
C2 - 8598392
AN - SCOPUS:0030059014
VL - 64
SP - 71
EP - 81
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
SN - 0165-5728
IS - 1
ER -