How IFNg can increase the expression of MHCI in vivo? what about in vitro?
Thanks
Hi
Both IFN alpha an dgamma increase Class I expression, but gamma is 8x more potent. By binding to the receptor on the cell surface, IFN activates NF-KB, which activates a series of Immune Regulatory Genes, including the promoter for Class I MHC. We saw up-regulation of Class I and II MHC (though lower than I), when we applied dengue virus supernatants to melanoma cells. The 624.28 line, however, has a deletion at HLA-A2, so only the B and C were elevated. IFN cannot restore Class I in the event of a deletion.
Bruce
Autoimmunity. 1992;12(1):13-9.
The effect of cytokines on the expression of MHC antigens and ICAM-1 by normal and transformed synoviocytes.
Wicks IP1, Leizer T, Wawryk SO, Novotny JR, Hamilton J, Vitti G, Boyd AW.
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Abstract
We report the expression on synovial cells of cell surface molecules known to be involved in T cell activation by antigen presenting cells. Normal human synovial fibroblasts and a human synovial cell line transformed with the SV40 large T antigen were used for in vitro stimulation studies with recombinant cytokines. We demonstrate an increase in MHC-A, B, C expression in normal synovial cells in response to recombinant interferon gamma (r gamma IFN), tumour necrosis factor alpha and beta (rTNF alpha and beta) and interleukin-1 (rIL-1 alpha). Intercellular adhesion molecular-1 (ICAM-1) expression was increased in parallel with MHC Class I. The combination of r gamma IFN and rTNF alpha was additive in its effect on ICAM-1 expression. Northern blot analysis suggests that ICAM-1 expression in synovial cells is controlled at the level of transcription. In contrast, MHC Class II (HLA-DR) was only significantly induced by r gamma IFN. Other stimuli including interleukin-4 (IL-4), interleukin 6 (IL-6), granulocyte macrophage colony stimulating factor (GM-CSF) and prostaglandin E2 (PGE2) did not affect the expression of ICAM-1 or MHC Class I and II. Leucocyte function antigen 3 (LFA-3) expression was not affected by any of the stimuli tested. Immunoperoxidase staining of rheumatoid synovial tissue confirmed enhanced in vivo expression of ICAM-1 in rheumatoid arthritis. These changes are discussed in the context of T cell activation in inflammatory arthritis.
PMID:
1352152
DOI:
10.3109/08916939209146125
Am J Pathol. 2001 Oct; 159(4): 1219–1224.
doi: 10.1016/S0002-9440(10)62507-2
PMCID: PMC1850521
In Vivo Expression of Major Histocompatibility Complex Molecules on Oligodendrocytes and Neurons during Viral Infection
Jeffrey M. Redwine, Michael J. Buchmeier, and Claire F. Evans
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Abstract
Demyelination in multiple sclerosis and in animal models is associated with infiltrating CD8+ and CD4+ T cells. Although oligodendrocytes and axons are damaged in these diseases, the roles T cells play in the demyelination process are not completely understood. Antigen-specific CD8+ T cell lysis of target cells is dependent on interactions between the T cell receptor and major histocompatibility complex (MHC) class I-peptide complexes on the target cell. In the normal central nervous system, expression of MHC molecules is very low but often increases during inflammation. We set out to precisely define which central nervous system cells express MHC molecules in vivo during infection with a strain of murine hepatitis virus that causes a chronic, inflammatory demyelinating disease. Using double immunofluorescence labeling, we show that during acute infection with murine hepatitis virus, MHC class I is expressed in vivo by oligodendrocytes, neurons, microglia, and endothelia, and MHC class II is expressed only by microglia. These data indicate that oligodendrocytes and neurons have the potential to present antigen to T cells and thus be damaged by direct antigen-specific interactions with CD8+ T lymphocytes.
Thank you so much for your answers :)
When this increase of MHCI can be detected which day after tumour cells injection?
Thanks again
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