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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5 || Follicle and follicular cells research abs 1 || Interferon research abs 1





Cancer Res. 2000 Dec 15;60(24):6800-4.
Identification of the interferon-inducible double-stranded RNA-dependent protein kinase as a regulator of cellular response to bulky adducts.

Bergeron J, Benlimame N, Zeng-Rong N, Xiao D, Scrivens PJ, Koromilas AE, Alaoui-Jamali MA.

Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital, Department of Medicine, McGill University, Montreal, Quebec, Canada.

The double-stranded RNA-dependent protein kinase PKR plays a central role in IFN-mediated antiviral response. The ability of PKR mutants to transform rodent fibroblasts led to the hypothesis that PKR acts as a tumor suppressor. Recent studies have identified an expanding network of PKR signaling partners, including signal transducers and activators of transcription 1 (STAT1), p53, and IkappaB-kinase. Here we demonstrate that PKR is involved in the cellular response to genotoxic stress. PKR-deficient mouse-embryonic fibroblasts (PKR-/-) are hypersensitive to bulky adduct DNA damage caused by cisplatin, melphalan, and UV radiation but not to other DNA-damaging agents such as Adriamycin. PKR-deficient cells are highly susceptible to cisplatin-induced apoptosis. They demonstrate retarded cisplatin adduct removal kinetics. Most strikingly, PKR localizes to the nucleus rapidly upon cisplatin treatment. Restoration of PKR in PKR-/- cells results in resistance to cisplatin and enhanced cell capacity to remove cisplatin DNA adducts. We conclude that PKR has a function in the regulation of cellular response to bulky adduct-inducing agents, possibly by modulating DNA repair mechanisms.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11156368&dopt=Abstract



Dis Colon Rectum. 2000 Dec;43(12):1754-8.
Expression of the SART1 tumor-rejection antigens in colorectal cancers.

Sasatomi T, Yamana H, Shichijo S, Tanaka S, Okamura T, Ogata Y, Itoh K, Shirouzu K.

Department of Immunology, Kurume University School of Medicine, Fukuoka, Japan.

PURPOSE: Colorectal cancer is one of the major causes of cancer death in the world, including in the United States and Japan. We recently identified the tumor-rejection antigen gene SART1, which encodes both the SART1(259) antigen expressed in the cytosol of epithelial cancers and the SART1(800) antigen expressed in the nucleus of the majority of proliferating cells. This study investigated the expression of these tumor antigens to explore a potential molecule for specific immunotherapy of colorectal cancer patients. METHODS: SART1 antigens were investigated by Western blotting in six colorectal cancer cell lines and in 33 colorectal cancer tissues. The cancer cell lines were tested for their ability to stimulate interferon-gamma production by the human-leukocyte-antigen-A24-restricted and SART1-specific cytotoxic T lymphocytes and were also tested for their susceptibility to the lysis by the cytotoxic T lymphocytes. RESULTS: The SART1(259) antigen was detected in the cytosol of four of six cancer cell lines, 13 of 33 (39 percent) cancer tissues, and 0 of 20 nontumorous colorectal tissues. The SART1(800) antigen was expressed in the nucleus of all the colorectal cancer cell lines, 18 of 33 (55 percent) cancer tissues, and 0 of 20 nontumorous tissues. The human-lymphocyte-antigen-A24-restricted and SART1-specific cytotoxic T lymphocytes killed the human-lymphocyte-antigen-A24+ SART1(259+) cancer cells. CONCLUSIONS: The SART1(259) antigen could be an appropriate target molecule for specific immunotherapy of approximately 40 percent of the human-lymphocyte-antigen-A24+ patients with colorectal cancer.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11156463&dopt=Abstract



Ann Rheum Dis. 2001 Feb;60(2):133-9.
Increased peripheral T cell reactivity to microbial antigens and collagen type II in rheumatoid arthritis after treatment with soluble TNFalpha receptors.

Berg L, Lampa J, Rogberg S, van Vollenhoven R, Klareskog L.

Department of Medicine, Unit of Rheumatology, Karolinska Institute, Stockholm, Sweden. louise.bermm.ki.se

OBJECTIVE: Peripheral T cells from patients with rheumatoid arthritis (RA) are hyporesponsive when stimulated with antigen or mitogen in vitro, possibly owing to increased production of proinflammatory cytokines such as tumour necrosis factor alpha (TNFalpha). This study sought to find out if and how RA T cell reactivity is affected during treatment with etanercept (Enbrel), a soluble TNFalpha receptor. METHODS: Heparinised blood was collected from patients with RA at baseline, after four and eight weeks of etanercept treatment, and from healthy controls. After density separation spontaneous production of interferon gamma (IFNgamma), TNFalpha, interleukin 6 (IL6), and IL10 by peripheral blood mononuclear cells (PBMC) was detected by ELISPOT. For detection of T cell reactivity, PBMC were stimulated in vitro with mitogen (phytohaemagglutinin (PHA)), microbial antigens (purified protein derivative (PPD), influenza), or an autoantigen, collagen type II (CII). Supernatants were analysed for IFNgamma and IL2 content by enzyme linked immunosorbent assay (ELISA). RESULTS: In RA the number of cells spontaneously producing IFNgamma was significantly increased after four, but not eight weeks' treatment with etanercept. T cell reactivity, as measured by IFNgamma production to PPD, influenza, and CII was significantly increased after four and sustained after eight weeks' treatment, whereas IFNgamma production induced by PHA remained unchanged. TNFalpha production was significantly higher in patients with RA than in controls and did not change during etanercept treatment. CONCLUSION: Treatment of patients with RA with etanercept may lead to increased peripheral T cell reactivity both to microbial antigens and to self antigens such as CII. These findings indicate that TNFalpha blockade may not only suppress but also stimulate certain aspects of antimicrobial immune defence and autoimmunity.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11156546&dopt=Abstract



Arterioscler Thromb Vasc Biol. 2001 Feb;21(2):227-32.
Induction of endothelial-leukocyte interaction by interferon-gamma requires coactivation of nuclear factor-kappaB.

De Caterina R, Bourcier T, Laufs U, La Fata V, Lazzerini G, Neish AS, Libby P, Liao JK.

Vascular Medicine Unit, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.

To determine whether nuclear factor (NF)-kappaB is necessary to confer endothelial cell responsiveness to interferon (INF)-gamma in terms of vascular cell adhesion molecule (VCAM)-1 expression and leukocyte adhesion, human endothelial cells were treated with IFN-gamma in the presence of low concentrations (LCs) of interleukin (IL)-1alpha (</=100 pg/mL), which activates NF-kappaB but does not induce VCAM-1 expression. Although IFN-gamma induced major histocompatibility complex class II antigen expression and although a high concentration of IL-1alpha (10 ng/mL) induced leukocyte adhesion and VCAM-1 expression, neither IFN-gamma nor LC IL-1alpha was able to induce VCAM-1 expression or leukocyte adhesion. However, the combination of IFN-gamma and LC IL-1alpha induced VCAM-1 expression and increased leukocyte adhesion (67% and 49% of high-concentration IL-1alpha, respectively). Electrophoretic mobility shift assays and immunoblotting of nuclear extracts showed that IFN-gamma activated signal transducers and activators of transcription (STAT)-1alpha and interferon regulatory factor (IRF)-1 but not NF-kappaB, whereas LC IL-1alpha activated NF-kappaB but not STAT-1alpha or IRF-1. Nuclear run-on studies showed that LC IL-1alpha is necessary but not sufficient for inducing VCAM-1 gene transcription and that the combination of IFN-gamma and LC IL-1alpha is required for full VCAM-1 gene transcription. These findings suggest that factors that activate NF-kappaB can synergize with IFN-gamma in promoting endothelial-leukocyte interaction.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11156857&dopt=Abstract



Circulation. 2001 Feb 6;103(5):756-61.
Cardioselective infection with coxsackievirus B3 requires intact type I interferon signaling: implications for mortality and early viral replication.

Wessely R, Klingel K, Knowlton KU, Kandolf R.

Deutsches Herzzentrum and 1 Medizinische Klinik, Technische Universitat, Munich, Germany.

BACKGROUND: Interferons (IFNs) play an important role in antiviral defense and have therapeutic potential in coxsackievirus heart disease. However, little is known about the relative contributions of type I and type II IFN signaling in coxsackievirus B3 (CVB3) infection or their role in the cardioselective nature of CVB3 infection. METHODS AND RESULTS: Wild-type mice and mice deficient for either the type I or the type II IFN receptor (IFNR) were infected with CVB3. Infection of the type I IFNR-deficient mice with >10(3) plaque-forming units (pfu) of CVB3 resulted in 100% mortality within 2 to 4 days after infection. Death was rare in wild-type and type II IFNR-deficient mice after inoculation with as much as 10(8) pfu of CVB3. Surprisingly, the early mortality in the type I IFNR-deficient mice was not accompanied by higher virus titers in the heart. Unexpectedly, a dramatic increase of viral RNA in the liver was found to correlate with early mortality in type I IFNR-deficient mice. CONCLUSIONS: Type I but not type II IFN signaling is essential for the prevention of early death due to CVB3 infection. Interestingly, neither type I or type II IFN signaling has a dramatic effect on early viral replication in the heart. However, lethal viral replication in the liver is controlled by type I IFNs. These results demonstrate that the IFN system is capable of modulating both viral pathogenicity and tissue tropism.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11156890&dopt=Abstract







The most ostensive feature that distinguishes us human from chimps and other primates is the lack of bodily hair. During evolutionary process, we have lost the majority of hair. Hair is no longer an essential part of our body, just like appendix. What little hair we still have on our scalp and a few other bodily parts is still regarded as significant for reasons other than biological necessity. Hair loss is naturally accompanied by aging process, although the extent of hair loss and the timing of onset vary widely among individuals. Thus, loss of hair and baldness is considered as a symbol of maturity or old age. Like winkles and other signs of aging, hair loss is not welcome by most people, because we don't welcome aging, and being perceived as an aging person. However, it is alopecia, or premature hair loss that especially concerns certain people.

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