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Blood. 2001 Feb 15;97(4):1056-62.
STAT3-mediated constitutive expression of SOCS-3 in cutaneous T-cell lymphoma.

Brender C, Nielsen M, Kaltoft K, Mikkelsen G, Zhang Q, Wasik M, Billestrup N, Odum N.

Institute of Medical Microbiology and Immunology, University of Copenhagen, Copenhagen, Denmark.

A characteristic feature of neoplastic transformation is the loss of external control by cytokines and extracellular matrix of cellular differentiation, migration, and mitogenesis. Because suppressors of cytokine signaling (SOCS) proteins are negative regulators of cytokine-induced signaling, it has been hypothesized that an aberrant SOCS expression plays a role in neoplastic transformation. This study reports on a constitutive SOCS-3 expression in cutaneous T-cell lymphoma (CTCL) cell lines. SOCS-3 protein is constitutively expressed in tumor cell lines (but not in nonmalignant T cells) obtained from affected skin from a patient with mycosis fungoides (MF) and from peripheral blood from a patient with Sezary syndrome (SS). In contrast, constitutive SOCS-3 expression is not found in the leukemic Jurkat T-cell line, the MOLT-4 acute lymphoblastic leukemia cell line, and the monocytic leukemic cell line U937. Expression of SOCS-3 coincides with a constitutive activation of STAT3 in CTCL tumor cells, and stable transfection of CTCL tumor cells with a dominant negative STAT3 strongly inhibits SOCS-3 expression, whereas transfection with wild-type STAT3 does not. Moreover, the reduced SOCS-3 expression in cells transfected with the dominant negative STAT3 is associated with an increased sensitivity to interferon-alpha (IFN-alpha). In conclusion, evidence is provided for a constitutive SOCS-3 expression in cancer cells obtained from patients with CTCL. Moreover, the findings indicate that the aberrant expression of SOCS-3 is mediated by a constitutive activation of STAT3 in CTCL cells and affects the IFN-alpha sensitivity of these cells. (Blood. 2001;97:1056-1062)

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11159537&dopt=Abstract

Blood. 2001 Feb 15;97(4):1123-30.
Prevention of lethal acute graft-versus-host disease in mice by oral administration of T helper 1 inhibitor, TAK-603.

Lu Y, Sakamaki S, Kuroda H, Kusakabe T, Konuma Y, Akiyama T, Fujimi A, Takemoto N, Nishiie K, Matsunaga T, Hirayama Y, Kato J, Kon S, Kogawa K, Niitsu Y.

Fourth Department of Internal Medicine and the First Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.

Acute graft-versus-host diseases (GVHD) is a major cause of morbidity and mortality in patients undergoing allogeneic bone marrow transplantation (BMT). T helper 1 (Th1)-type cytokines such as interferon-gamma or tumor necrosis factor-alpha have been implicated in the pathogenesis of acute GVHD. TAK-603 is a new quinoline derivative, which is now in clinical trials for use as a disease-modifying antirheumatic drug. In preclinical studies, it inhibited delayed-type hypersensitivity, but not Arthus-type reaction, in mice, and selectively suppressed Th1 cytokine production. Thus, the present study was designed to investigate whether the Th1 inhibitor (TAK-603) ameliorates lethal acute GVHD in a mouse model. Administration of TAK-603 into BALB/c mice given 10 Gy total body irradiation followed by transplantation of bone marrow and spleen cells from C57BL/6 mice markedly reduced the mortality in association with minimal signs of GVHD pathology in the liver, intestine, and skin. TAK-603 reduced not only the production of Th1-type cytokines, but also the proportion of Th1 cells in CD4(+) helper T cells in this GVHD mouse model. These results suggest that TAK-603 could be a potent therapeutic agent for acute lethal GVHD.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11159546&dopt=Abstract

Br J Pharmacol. 2001 Jan;132(2):419-26.
Impaired response to interferon-gamma in activated macrophages due to tyrosine nitration of STAT1 by endogenous nitric oxide.

Llovera M, Pearson JD, Moreno C, Riveros-Moreno V.

Centre for Cardiovascular Biology & Medicine, School of Biomedical Sciences, King's College London, Guy's Campus, London SE1 1UL.

1.Inducible NO synthase (iNOS) expression and activity were measured in the mouse macrophage cell line J774 after exposure to bacterial lipopolysaccharide (LPS) with or without interferon-gamma (IFN-gamma). 2. Inhibition of NOS activity by concomitant N(G)-monomethyl-L-arginine (L-NMMA) treatment further increased iNOS protein levels, with a substantial increase in iNOS half-life. 3. Western blotting and ELISA demonstrated that several cell proteins were tyrosine-nitrated when iNOS activity was high. 4. Rapid IFN-gamma-induced phosphorylation of STAT1 was reduced by about 40% when cells were pretreated to induce iNOS, unless L-NMMA was present during the pretreatment period. 2D gel electrophoresis demonstrated the presence of nitrotyrosine in STAT1 after iNOS induction, and confirmed the reduction in phospho-STAT1 on subsequent stimulation with IFN-gamma for 15 min and its partial restoration when L-NMMA was present during the pretreatment period. 5. We did not detect tyrosine nitration of the upstream kinase JAK2 in LPS+IFN-gamma pretreated cells, but JAK2 activity was also impaired, and was partially restored by concomitant L-NMMA pretreatment. 6. We conclude that endogenous production of NO induces feedback inhibition of signalling pathways activated by IFN-gamma, at least in part by nitrating tyrosine residues in STAT1 which prevents phosphorylation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11159690&dopt=Abstract

Endocrinology. 2001 Feb;142(2):823-9.
Pregnancy and murine thyroiditis: thyroglobulin immunization leads to fetal loss in specific allogeneic pregnancies.

Imaizumi M, Pritsker A, Kita M, Ahmad L, Unger P, Davies T.

Division of Endocrinology and Metabolism, Department of Medicine , New York, New York 10029, USA.

Thyroid autoantibodies are risk factors in human pregnancy. To investigate the influence of autoimmune thyroiditis on pregnancy, we have studied the impact of murine experimental autoimmune thyroiditis (EAT) on pregnancy outcome by using thyroglobulin (Tg) immunized CBA/J (H2(k)) female mice. When Tg immunized mice were mated with BALB/c (H2(d)) males, only 57% (47/83) of pregnant mice maintained their conceptions compared with >85% of other strain combinations (P < 0.05). We also found that MHC class II antigens were expressed on placental cells from Tg immunized pregnant mice but not in control normal pregnancies. Furthermore, the frequency and severity of thyroiditis, assessed by histological analyses, was also increased in Tg immunized mice mated with the BALB/c strain compared with syngeneic pregnancies (P < 0.05). In these pregnant mice mated with BALB/c, interleukin-4 secretion by mitogen-stimulated spleen cells was significantly suppressed and interferon-gamma secretion by mixed lymphocyte reactions with BALB/c cells was significantly increased. These data demonstrated enhanced Th1 cell proliferation and fetal loss in CBA/J X BALB/c pregnancies. We concluded, therefore, that pregnancy loss was increased in experimental autoimmune thyroiditis in a manner that was dependent on paternal antigens. These observations have broad implications for understanding the immunology of pregnancy.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11159855&dopt=Abstract

Infect Immun. 2001 Feb;69(2):665-72.
Influence of costimulatory molecules on immune response to Leishmania major by human cells in vitro.

Brodskyn CI, DeKrey GK, Titus RG.

Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado 80523, USA.

The importance of CD40, CD80, and CD86 costimulatory molecules in anti-Leishmania immune responses has been established in murine models. A role for these costimulatory molecules in human anti-Leishmania immune responses was investigated in this study. Autologous macrophages and peripheral blood leukocytes (PBL) were prepared from peripheral blood mononuclear cells of Leishmania-naive donors and cultured with or without Leishmania major in various combinations. After 7 days of culture, high levels of CD40 and CD86 were expressed on macrophages in the presence or absence of L. major. When macrophages were cultured for an additional 7 days with PBL, expression of all three costimulatory molecules was detected. When L. major was present in these cultures, the expression of CD80, and to a lesser extent CD40, on macrophages was enhanced. Blockade of CD80, CD86, or both molecules (in the order of greatest effect) in cultures containing macrophages, PBL, and L. major significantly inhibited the production of gamma interferon, interleukin-5 (IL-5), and IL-12. Blockade of CD40-CD154 interactions also significantly inhibited production of these cytokines in response to L. major. Production of IL-10 was unaltered by the blockade of these costimulatory molecules. Thus, these data suggest that CD40, CD80, and CD86 expression and regulation may significantly impact anti-Leishmania immune responses in humans.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11159953&dopt=Abstract

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