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Mutational analysis of TNF-alpha gene reveals a regulatory role for the 3'-untranslated region in the genetic predisposition to lupus-like autoimmune disease

Autor: C O Jacob, S K Lee, G Strassmann

Publikováno v: The Journal of Immunology. 156:3043-3050

Lupus-prone mice show reduced production of TNF-alpha and, upon long-term treatment with recombinant TNF-alpha, significant protection from disease development. Mutational analysis of the 5'-untranslated region (UTR) and 3'-UTR of the mouse TNF-alpha

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::6bb0275235d4559b6060ad3400980874
https://doi.org/10.4049/jimmunol.156.8.3043

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Cyclic nucleotide phosphodiesterase type IV participates in the regulation of IL-10 and in the subsequent inhibition of TNF-alpha and IL-6 release by endotoxin-stimulated macrophages

Autor: T Kambayashi, C O Jacob, D Zhou, N Mazurek, M Fong, G Strassmann

Publikováno v: The Journal of Immunology. 155:4909-4916

We have recently shown that PGE2 inhibits the release of TNF-alpha from LPS-stimulated murine peritoneal macrophages via a feedback mechanism involving IL-10. Here we demonstrate that a rolipram-sensitive phosphodiesterase (PDE) type IV participates

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::cec941430a96b00831238dac78d8f7e1
https://doi.org/10.4049/jimmunol.155.10.4909

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Mechanisms of experimental cancer cachexia. Interaction between mononuclear phagocytes and colon-26 carcinoma and its relevance to IL-6-mediated cancer cachexia

Autor: G Strassmann, C O Jacob, R Evans, D Beall, M Fong

Publikováno v: The Journal of Immunology. 148:3674-3678

In a recent report we showed that IL-6 is an important mediator of experimental cancer cachexia in the colon-26 (C-26) tumor system. In culture, on a per cell basis, C-26.IVX cell line (which develops tumors and induces severe cachexia of syngeneic h

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::1272b5b9d26c7f5fddf1507f4a5349be
https://doi.org/10.4049/jimmunol.148.11.3674

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Polymorphisms in the tumor necrosis factor alpha (TNF-alpha) gene correlate with murine resistance to development of toxoplasmic encephalitis and with levels of TNF-alpha mRNA in infected brain tissue

Autor: Jack S. Remington, C O Jacob, Yasuhiro Suzuki, G Sgarlato, Yvonne R. Freund

Publikováno v: The Journal of Experimental Medicine

Murine resistance to development of toxoplasmic encephalitis (TE) has recently been mapped to the D region of the major histocompatibility complex (H-2). Since the gene for tumor necrosis factor alpha (TNF-alpha) is located 5' of the D region and TNF

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::35155c2a0ec55b832172f4911e859d9b
https://doi.org/10.1084/jem.175.3.683

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Regulation of MHC class II antigen expression. Opposing effects of tumor necrosis factor-alpha on IFN-gamma-induced HLA-DR and Ia expression depends on the maturation and differentiation stage of the cell

Autor: Y Watanabe, C O Jacob

Publikováno v: The Journal of Immunology. 146:899-905

MHC class II induction by cytokines has been suggested to play a major role in the initiation and propagation of immune and autoimmune processes. TNF-alpha has been found both to enhance and also to inhibit IFN-gamma-induced MHC class II expression.

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::03e9fe21f24033abecef892d0877a7c7
https://doi.org/10.4049/jimmunol.146.3.899

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Synergistic effect between IL-10 and bcl-2 genotypes in determining susceptibility to systemic lupus erythematosus

Autor: R, Mehrian, F P, Quismorio, G, Strassmann, M M, Stimmler, D A, Horwitz, R C, Kitridou, W J, Gauderman, J, Morrison, C, Brautbar, C O, Jacob

Publikováno v: Arthritis and rheumatism. 41(4)

To determine whether genes participating in programmed cell death, including bcl-2, IL-10, Fas-L, and CTLA-4, may contribute to the genetic predisposition to systemic lupus erythematosus (SLE).First, intragenic markers for the bcl-2, IL-10, Fas-L, an

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=pmid________::6b60d1868a9f5f8a15b4a1f331324863
https://pubmed.ncbi.nlm.nih.gov/9550468

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Impaired nonrestricted cytolytic activity in systemic lupus erythematosus: involvement of a pathway independent of Fas, tumor necrosis factor, and extracellular ATP that is associated with little detectable perforin

Autor: W, Stohl, J E, Elliott, L, Li, E R, Podack, D H, Lynch, C O, Jacob

Publikováno v: Arthritis and rheumatism. 40(6)

To determine the cytolytic effector pathway involved in impaired generation of nonrestricted cytolytic activity in systemic lupus erythematosus (SLE).Peripheral blood mononuclear cells (PBMC) from normal subjects and SLE patients were stimulated in v

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=pmid________::034a90546f2140425f24edaba6ca4650
https://pubmed.ncbi.nlm.nih.gov/9182924

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Genetic variability in tumor necrosis factor production: relevance to predisposition to autoimmune disease

Autor: C O, Jacob

Publikováno v: Regional immunology. 4(5)

Rather than being involved merely in the effector arm of inflammatory processes that contribute to autoimmune organ destruction, a primary involvement of TNF may be in some of the more basic mechanisms that occur in autoimmune disease. In this review

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=pmid________::8739a1173d411f2dcac7b52bff2d02fc
https://pubmed.ncbi.nlm.nih.gov/1290749

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Tumor necrosis factor and interferon gamma: relevance for immune regulation and genetic predisposition to autoimmune disease

Autor: C O, Jacob

Publikováno v: Seminars in immunology. 4(3)

The role of TNF-alpha and IFN-gamma in various models of autoimmune disease were analyzed. These include murine models of lupus, type 1 diabetes in NOD mice and the adjuvant arthritis model in rats. Rather than being involved mainly in the effector a

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=pmid________::487a7834b7c0bc2dd9165c135f64d788
https://pubmed.ncbi.nlm.nih.gov/1627786

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