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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

Placenta. 1999 Mar-Apr;20(2-3):197-202.
Placental release of corticotrophin-releasing hormone across the umbilical circulation of the human newborn.

Nodwell A, Carmichael L, Fraser M, Challis J, Richardson B.

Department of Obstetrics and Gynaecology, University of Western Ontario, London, Canada.

This study attempted to determine the placental release of corticotrophin-releasing hormone (CRH) into the umbilical circulation, and the factors which affect it, by measuring venous and arterial levels for CRH across the umbilical circulation in labouring as well as non-labouring elective caesarean section patients. The relationship with measures of fetal oxygenation and acid-base status at birth was investigated also. Forty-eight patients were studied (term labour n = 30, term elective caesarean section n = 12, and preterm labour n = 6) with blood sampling from a clamped segment of cord after delivery of the fetus and from the cord at its insertion into the placenta after delivery of the placenta, with subsequent measurement of blood gases, pH, base excess, and CRH. For all patients, mean plasma CRH levels in the umbilical and placental vein (115+/-13 and 145+/-18 pg/ml) were higher than those from the corresponding artery (85+/-7 and 102+/-8 pg/ml, P<0.01 and P<0.05, respectively), indicating placental release of CRH into the fetal compartment. In addition, placental venous and arterial cord CRH levels were higher than those from the corresponding umbilical levels (P<0.01 and P<0.02, respectively) indicating continued placental release of CRH into blood within the placenta after clamping of the umbilical circulation and delivery of the fetus. While plasma CRH levels from respective cord vessels were all significantly higher in labouring patients at term versus elective caesarean section patients, there were no differences compared with preterm labouring patients. For all patients, CRH as measured in both the umbilical and placental vein showed a modest inverse correlation to base excess as measured in the umbilical artery, -0.31 and -0.33, respectively, both P<0.05. It is concluded that CRH is released by the placenta into the fetal compartment and is increased with both term and preterm labour, and with metabolic acidosis during labour, supporting a role in the endocrine events of labour and/or compensatory changes in uteroplacental blood flow.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10195742&dopt=Abstract

Mol Cell Biol. 2002 Nov;22(22):7929-41.
Glucocorticoid-induced leucine zipper inhibits the Raf-extracellular signal-regulated kinase pathway by binding to Raf-1.

Ayroldi E, Zollo O, Macchiarulo A, Di Marco B, Marchetti C, Riccardi C.

Department of Clinical and Experimental Medicine, Section of Pharmacology. Department of Drug Chemistry and Technology, University of Perugia, 06100 Perugia, Italy.

Glucocorticoid-induced leucine zipper (GILZ) is a leucine zipper protein, whose expression is augmented by dexamethasone (DEX) treatment and downregulated by T-cell receptor (TCR) triggering. Stable expression of GILZ in T cells mimics some of the effects of glucocorticoid hormones (GCH) in GCH-mediated immunosuppressive and anti-inflammatory activity. In fact, GILZ overexpression inhibits TCR-activated NF-kappaB nuclear translocation, interleukin-2 production, FasL upregulation, and the consequent activation-induced apoptosis. We have investigated the molecular mechanism underlying GILZ-mediated regulation of T-cell activation by analyzing the effects of GILZ on the activity of mitogen-activated protein kinase (MAPK) family members, including Raf, MAPK/extracellular signal-regulated kinase (ERK) 1/2 (MEK-1/2), ERK-1/2, and c-Jun NH(2)-terminal protein kinase (JNK). Our results indicate that GILZ inhibited Raf-1 phosphorylation, which resulted in the suppression of both MEK/ERK-1/2 phosphorylation and AP-1-dependent transcription. We demonstrate that GILZ interacts in vitro and in vivo with endogenous Raf-1 and that Raf-1 coimmunoprecipitated with GILZ in murine thymocytes treated with DEX. Mapping of the binding domains and experiments with GILZ mutants showed that GILZ binds the region of Raf interacting with Ras through the NH(2)-terminal region. These data suggest that GILZ contributes, through protein-to-protein interaction with Raf-1 and the consequent inhibition of Raf-MEK-ERK activation, to regulating the MAPK pathway and to providing a further mechanism underlying GCH immunosuppression.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12391160&dopt=Abstract

Mol Cell Biol. 2002 Nov;22(22):8035-43.
Inactivation of the F4/80 glycoprotein in the mouse germ line.

Schaller E, Macfarlane AJ, Rupec RA, Gordon S, McKnight AJ, Pfeffer K.

Institute of Medical Microbiology, Immunology and Hygiene, Technical University of Munich, D-81675 Munich, Germany.

Macrophages play a crucial role in the defense against pathogens. Distinct macrophage populations can be defined by the expression of restricted cell surface proteins. Resident tissue macrophages, encompassing Kupffer cells of the liver and red pulp macrophages of the spleen, characteristically express the F4/80 molecule, a cell surface glycoprotein related to the seven transmembrane-spanning family of hormone receptors. In this study, gene targeting was used to simultaneously inactivate the F4/80 molecule in the germ line of the mouse and to produce a mouse line that expresses the Cre recombinase under the direct control of the F4/80 promoter (F4/80-Cre knock-in). F4/80-deficient mice are healthy and fertile. Macrophage populations in tissues can develop in the absence of F4/80 expression. Functional analysis revealed that the generation of T-cell-independent B-cell responses and macrophage antimicrobial defense after infection with Listeria monocytogenes are not impaired in the absence of F4/80. Interestingly, tissues of F4/80-deficient mice could not be labeled with anti-BM8, another macrophage subset-specific marker with hitherto undefined molecular antigenic structure. Recombinant expression of a F4/80 cDNA in heterologous cells confirmed this observation, indicating that the targets recognized by the F4/80 and BM8 monoclonal antibodies are identical.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12391169&dopt=Abstract

J Immunol. 2002 Nov 1;169(9):4840-9.
High-affinity HLA-A(*)02.01 peptides from parathyroid hormone-related protein generate in vitro and in vivo antitumor CTL response without autoimmune side effects.

Francini G, Scardino A, Kosmatopoulos K, Lemonnier FA, Campoccia G, Sabatino M, Pozzessere D, Petrioli R, Lozzi L, Neri P, Fanetti G, Cusi MG, Correale P.

Division of Medical Oncology, Institut National de la Sante et de la Recherche Medicale Unite d'Immunite Cellulaire Antivirale, Institut Pasteur, Paris, France. francinnisi.it

Parathyroid hormone-related protein (PTH-rP), a protein produced by prostate carcinoma and other epithelial cancers, is a key agent in the development of bone metastases. We investigated whether the protein follows the self-tolerance paradigm or can be used as a target Ag for anticancer immunotherapy by investigating the immunogenicity of two HLA-A(*)02.01-binding PTH-rP-derived peptides (PTR-2 and -4) with different affinity qualities. PTH-rP peptide-specific CTL lines were generated from the PBMC of two HLA-A(*)02.01(+) healthy individuals, stimulated in vitro with PTH-rP peptide-loaded autologous dendritic cells and IL-2. The peptide-specific CTLs were able to kill PTH-rP(+)HLA-A(*)02.01(+) breast and prostate carcinoma cell lines. The two peptides were also able to elicit a strong antitumor PTH-rP-specific CTL response in HLA-A(*)02.01 (HHD) transgenic mice. The vaccinated mice did not show any sign of side effects due to cell-mediated autoimmunity or toxicity. In this study we describe two immunogenic and toxic-free PTH-rP peptides as valid candidates for the design of peptide-based vaccination strategies against prostate cancer and bone metastases from the most common epithelial malignancies.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12391194&dopt=Abstract

J Immunol. 2002 Nov 1;169(9):4905-12.
Highly immunogenic and totally synthetic lipopeptides as self-adjuvanting immunocontraceptive vaccines.

Zeng W, Ghosh S, Lau YF, Brown LE, Jackson DC.

Cooperative Research Center for Vaccine Technology, Department of Microbiology and Immunology, University of Melbourne, Parkville, Victoria, Australia.

In this study, we describe the synthesis of various lipopeptides based on the sequence of luteinizing hormone-releasing hormone (LHRH) and report on their abilities to induce Abs against this "self" hormone when inoculated into mice in the absence of additional adjuvant. The peptides consisted of a colinear CD4(+) T helper cell epitope from the L chain of influenza virus hemagglutinin and LHRH, which has B cell epitopes but no T cell epitopes present in its sequence. Lipids were attached either at the N terminus or between the T cell epitope and LHRH, in the approximate center of the peptide. The lipopeptide constructs displayed different solubilities and immunological properties that depended not only on the lipid content but also on the position of attachment of the lipids. Some of these constructs were highly immunogenic, inducing high titers of Ab, which were capable of efficiently sterilizing female mice when administered in saline by s.c. or intranasal routes. The most effective vaccines were highly soluble, contained the dipalmitoyl-S-glyceryl cysteine moiety, and had this lipid attached at the center of the molecule. The relative ability of the lipopeptides to induce an Ab response in the absence of external adjuvant was reflected by their ability to up-regulate the surface expression of MHC class II molecules on immature dendritic cells. These results demonstrate that the composition and position within peptide vaccines of self-adjuvanting lipid groups can influence the ability to induce the maturation of dendritic cells and, in turn, the magnitude of the resulting Ab response.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12391202&dopt=Abstract

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