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Biochem Biophys Res Commun. 2003 Apr 25;304(1):143-7.
p21waf1/cip1 is down-regulated in conjunction with up-regulation of c-Fos in the lymphocytes of rheumatoid arthritis patients.

Hikasa M, Yamamoto E, Kawasaki H, Komai K, Shiozawa K, Hashiramoto A, Miura Y, Shiozawa S.

Department of Rheumatology, Faculty of Health Science, Kobe University School of Medicine, 654-0142, Kobe, Japan.

Features characteristic to rheumatoid arthritis (RA) including synovial overgrowth and joint destruction are experimentally produced by augmenting c-fos gene expression. We show that cyclin dependent kinase inhibitor p21waf1/cip1, that inhibits cell proliferation, is down-regulated in conjunction with up-regulation of c-fos in the lymphocytes of patients with RA. As to the mechanism of down-regulation of p21waf1/cip1 gene expression, transfection studies in U937 cells showed that c-fos down-regulated phosphorylation and dimerization of signal transducers and activators of transcription (STAT) 1, thereby inhibiting interferon -induced transactivation of p21waf1/cip1. Phosphorylation of STAT1 was indeed decreased in the lymphocytes of patients with RA. Thus, under overexpression of c-fos gene, c-Fos inactivates STAT1 to down-regulate p21waf1/cip1 gene expression in the lymphocytes of patients with RA, and in this way may enhance proliferation of lymphocytes.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12705898&dopt=Abstract

Digestion. 2001;63 Suppl 1:37-42.
Interleukin-18 and Crohn's disease.

Kanai T, Watanabe M, Okazawa A, Sato T, Hibi T.

Keio Cancer Center, School of Medicine, Keio University, Keio, Japan.

The etiology and pathogenesis of inflammatory bowel disease remains an area under intense investigation. Crohn's disease (CD) is characterized by a marked accumulation of activated Th1 type CD4+ T cells and macrophages in inflamed intestinal mucosa. IL-18 is a recently described cytokine that mainly exists in activated macrophages and shares biological activities with IL-12 in driving the development of Th1 type CD4+ T cells by inducing interferon-gamma. To clarify the role of IL-18 in intestinal inflammation in CD, we assessed the functional role of IL-18 in regulating intestinal mucosal lymphocytes in human CD and murine CD model. 2001 S. Karger AG, Basel

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11173908&dopt=Abstract

Kidney Blood Press Res. 2001;24(1):27-32.
IL-12-dependent, INF-gamma-independent experimental glomerulonephritis.

Le Hir M, Ryffel B, Schatzmann U.

Institute of Anatomy, University of Zurich, Switzerland. lehinatom.unizh.ch

There is evidence that crescentic glomerulonephritis initiated in rodents by heterologous antibodies against the glomerular basement membrane (anti-GBM glomerulonephritis) depends on a Th1-type immune reaction. Interleukin 12 (IL-12) is crucial for the development of Th1 helper cells, and interferon gamma (IFN-gamma) is a major proinflammatory product of these cells. In order to test the role of the two cytokines in anti-GBM glomerulonephritis we used mice lacking either the p40 chain of IL-12 (IL-12-/-) or the IFN-gamma receptor (IFN-gammaR-/-). Glomerulonephritis was induced by injecting a rabbit anti-GBM serum in mice preimmunized against rabbit IgG. Glomerulonephritis was assessed on the basis of proteinuria, immunofluorescence findings and histology. IL-12-/- mice were completely protected against glomerulonephritis. In contrast, IFN-gammaR-/- mice were more severely affected than wild-type mice. Similarly, cutaneous delayed-type hypersensitivity, a typical Th1 response, was abolished in the IL-12-/-, mice but increased in the IFN-gammaR-/- mice. The data obtained in IL-12-/- mice support the view that crescentic glomerulonephritis in this model represents a Th1 response. Since IFN-gamma is not required, other products of Th1 cells are likely to mediate glomerulonephritis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11174003&dopt=Abstract

Eur J Dermatol. 2001 Jan-Feb;11(1):48-9.
Erythema induratum in a patient with active tuberculosis of the axillary lymph node: IFN-gamma release of specific T cells.

Koga T, Kubota Y, Kiryu H, Nakayama J, Matsuzoe D, Shirakusa T.

Department of Dermatology, School of Medicine, Fukuoka University, 3-1-1, Maidashi, Higashi-ku, J-812-8582 Fukuoka, Japan. tekogermatol.med.kyushu-u.ac.jp

A 57-year-old woman with tender nodular lesions on her legs, arms, buttocks and face is reported as a case of erythema induratum (EI) with active tuberculosis of axillary lymph nodes. Both skin nodular lesions and lymph nodes responded positively to antituberculous therapy. The patient's peripheral blood mononuclear cells showed a high proliferation and produced interferon-gamma (IFN-gamma) in response to purified protein derivative (PPD). These findings indicate the possibility that PPD-specific T cells, capable of producing IFN-gamma, are likely to be involved in the formation of EI as a type of delayed-type hypersensitivity response to mycobacterial antigens at the site of skin lesions.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11174139&dopt=Abstract

Cell Death Differ. 2000 Dec;7(12):1244-52.
Regulation of Bcl-2-family proteins in myeloma cells by three myeloma survival factors: interleukin-6, interferon-alpha and insulin-like growth factor 1.

Jourdan M, De Vos J, Mechti N, Klein B.

INSERM U475 and Unit for Cellular Therapy, CHU Montpellier, 34197 Montpellier, France.

As survival regulation is a key process in multiple myeloma biology, we have studied the Bcl-2 family proteins that can be regulated by three myeloma cell survival factors: interleukin-6 (IL-6), interferon-alpha (IFN-alpha) and insulin-like growth factor (IGF-1). Eleven myeloma cell lines, whose survival and proliferation are dependent on addition of IL-6, variably expressed 10 anti-apoptotic or pro-apoptotic proteins of the Bcl-2-family. When myeloma cells from four cell lines were IL-6 starved and activated with IL-6 or IFN-alpha, we observed that only Mcl-1 expression was up-regulated with myeloma cell survival induction. Nor was obvious regulation of these 10 pro-apoptotic or anti-apoptotic proteins found with IGF-1, another potent myeloma cell survival factor. Our results indicate that the myeloma cell survival activity of IL-6 linked to Bcl-xL regulation cannot be generalized and emphasize that Mcl-1 is the main target of IL-6 and IFN-alpha stimulation. However, other changes in the activity of the Bcl-2 protein family or other apoptosis regulators must be identified to elucidate the IGF-1 action mechanism. Cell Death and Differentiation (2000) 7, 1244 - 1252.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11175262&dopt=Abstract

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