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16. CD200 receptor restriction of myeloid cell responses antagonizes antiviral immunity and facilitates cytomegalovirus persistence within mucosal tissue

Author

Stack, G, Jones, E, Marsden, M, Stacey, MA, Snelgrove, RJ, Lacaze, P, Jacques, LC, Cuff, SM, Stanton, RJ, Gallimore, AM, Hussell, T, Wilkinson, GWG, Ghazal, P, Taylor, PR, and Humphreys, IR

Subjects
DOWN-REGULATION, HOST, Lymphocyte, viruses, PROTEIN, Cytomegalovirus, Fluorescent Antibody Technique, MACROPHAGE ACTIVATION, Mice, 0302 clinical medicine, 1108 Medical Microbiology, INFLUENZA INFECTION, Biology (General), Receptor, Oligonucleotide Array Sequence Analysis, Mice, Knockout, 0303 health sciences, Membrane Glycoproteins, Effector, Flow Cytometry, 3. Good health, medicine.anatomical_structure, 1107 Immunology, Cytomegalovirus Infections, MOUSE-CYTOMEGALOVIRUS, medicine.symptom, Life Sciences & Biomedicine, 0605 Microbiology, Research Article, QH301-705.5, SALIVARY-GLANDS, Immunology, Congenital cytomegalovirus infection, Inflammation, VIRUS-INFECTION, Biology, Microbiology, 03 medical and health sciences, INFLAMMATION, Downregulation and upregulation, Antigens, CD, Virology, Genetics, medicine, Animals, Molecular Biology, 030304 developmental biology, MURINE CYTOMEGALOVIRUS, Science & Technology, Innate immune system, Mucous Membrane, Macrophages, RC581-607, medicine.disease, R1, Mice, Inbred C57BL, Disease Models, Animal, Viral replication, Parasitology, Immunologic diseases. Allergy, 030215 immunology
Abstract

CD200 receptor (CD200R) negatively regulates peripheral and mucosal innate immune responses. Viruses, including herpesviruses, have acquired functional CD200 orthologs, implying that viral exploitation of this pathway is evolutionary advantageous. However, the role that CD200R signaling plays during herpesvirus infection in vivo requires clarification. Utilizing the murine cytomegalovirus (MCMV) model, we demonstrate that CD200R facilitates virus persistence within mucosal tissue. Specifically, MCMV infection of CD200R-deficient mice (CD200R-/-) elicited heightened mucosal virus-specific CD4 T cell responses that restricted virus persistence in the salivary glands. CD200R did not directly inhibit lymphocyte effector function. Instead, CD200R-/- mice exhibited enhanced APC accumulation that in the mucosa was a consequence of elevated cellular proliferation. Although MCMV does not encode an obvious CD200 homolog, productive replication in macrophages induced expression of cellular CD200. CD200 from hematopoietic and non-hematopoietic cells contributed independently to suppression of antiviral control in vivo. These results highlight the CD200-CD200R pathway as an important regulator of antiviral immunity during cytomegalovirus infection that is exploited by MCMV to establish chronicity within mucosal tissue., Author Summary Immune inhibitory receptors, including CD200 receptor (CD200R), can limit immune responses in the mucosa to restrict reactivity to the plethora of harmless antigens that mucosal surfaces are continually exposed to. However, viruses may exploit these suppressive mechanisms to enable their persistence and spread. Many viruses, including herpesviruses, have acquired functional homologs of CD200, the ligand of CD200R, implying that viral exploitation of this pathway is evolutionary advantageous. We now show that the β-herpesvirus murine cytomegalovirus (MCMV) takes advantage of the CD200R inhibitory pathway to persist within a mucosal site of MCMV persistence, the salivary glands. Mice deficient in CD200R mounted elevated antiviral immune responses that were driven by the increased division and accumulation of myeloid cells that function to orchestrate the generation of antiviral effector immune responses. Interestingly, MCMV infection of myeloid cells up-regulated CD200 expression. Thus, MCMV exploits the CD200 pathway to persist within mucosal tissue.

Published
2015
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17. The role of IL-22 in viral infections: Paradigms and paradoxes

Author

Gimeno Brias, S., Stack, G., Stacey, M.A., Redwood, A.J., Humphreys, I.R., Gimeno Brias, S., Stack, G., Stacey, M.A., Redwood, A.J., and Humphreys, I.R.

Abstract

Interleukin-22 (IL-22) is a member of the IL-10 family of cytokines. Hematopoietic cells express IL-22, and this cytokine signals through the heterodimeric IL-22 receptor expressed by non-hematopoietic cells. A growing body of evidence points toward a role for IL-22 in a diverse array of biological functions ranging from cellular proliferation, tissue protection and regeneration, and inflammation. In recent years, the role that IL-22 plays in antiviral immune responses has been examined in a number of infection models. Herein, we assess our current understanding of how IL-22 determines the outcome of viral infections and define common mechanisms that are evident from, sometimes paradoxical, findings derived from these studies. Finally, we discuss the potential therapeutic utility of IL-22 manipulation in the treatment and prevention of viral infections and associated pathologies.

Published
2016

18. Neutrophils recruited by IL-22 in peripheral tissues function as TRAIL-dependent antiviral effectors against MCMV

Author

Stacey, M, Marsden, M, Pham N, T, Clare, S, Dolton, G, Stack, G, Jones, E, Klenerman, P, Gallimore, A, Taylor, P, Snelgrove, R, Lawley, T, Dougan, G, Benedict, C, Jones, SA, Wilkinson, G, and Humphreys, I

Abstract

During primary infection, murine cytomegalovirus (MCMV) spreads systemically, resulting in virus replication and pathology in multiple organs. This disseminated infection is ultimately controlled, but the underlying immune defense mechanisms are unclear. Investigating the role of the cytokine IL-22 in MCMV infection, we discovered an unanticipated function for neutrophils as potent antiviral effector cells that restrict viral replication and associated pathogenesis in peripheral organs. NK-, NKT-, and T cell-secreted IL-22 orchestrated antiviral neutrophil-mediated responses via induction in stromal nonhematopoietic tissue of the neutrophil-recruiting chemokine CXCL1. The antiviral effector properties of infiltrating neutrophils were directly linked to the expression of TNF-related apoptosis-inducing ligand (TRAIL). Our data identify a role for neutrophils in antiviral defense, and establish a functional link between IL-22 and the control of antiviral neutrophil responses that prevents pathogenic herpesvirus infection in peripheral organs.

Published
2014

20. Neutrophils Recruited by IL-22 in Peripheral Tissues Function as TRAIL-Dependent Antiviral Effectors against MCMV

Author

Stacey, MA, Marsden, M, Pham, TAN, Clare, S, Dolton, G, Stack, G, Jones, E, Klenerman, P, Gallimore, AM, Taylor, PR, Snelgrove, RJ, Lawley, TD, Dougan, G, Benedict, CA, Jones, SA, Wilkinson, GWG, Humphreys, IR, Stacey, MA, Marsden, M, Pham, TAN, Clare, S, Dolton, G, Stack, G, Jones, E, Klenerman, P, Gallimore, AM, Taylor, PR, Snelgrove, RJ, Lawley, TD, Dougan, G, Benedict, CA, Jones, SA, Wilkinson, GWG, and Humphreys, IR

Abstract

During primary infection, murine cytomegalovirus (MCMV) spreads systemically, resulting in virus replication and pathology in multiple organs. This disseminated infection is ultimately controlled, but the underlying immune defense mechanisms are unclear. Investigating the role of the cytokine IL-22 in MCMV infection, we discovered an unanticipated function for neutrophils as potent antiviral effector cells that restrict viral replication and associated pathogenesis in peripheral organs. NK-, NKT-, and T cell-secreted IL-22 orchestrated antiviral neutrophil-mediated responses via induction in stromal nonhematopoietic tissue of the neutrophil-recruiting chemokine CXCL1. The antiviral effector properties of infiltrating neutrophils were directly linked to the expression of TNF-related apoptosis-inducing ligand (TRAIL). Our data identify a role for neutrophils in antiviral defense, and establish a functional link between IL-22 and the control of antiviral neutrophil responses that prevents pathogenic herpesvirus infection in peripheral organs.

Published
2014

21. LIST OF CONTRIBUTORS AND DISCUSSANTS

Author

Ahmed, C.E., primary, Albertson, B.D., additional, Andreone, T., additional, Anogianakis, G., additional, Asa, S., additional, Atlas, S.A., additional, Aurbach, G.D., additional, Baird, A., additional, Bardin, C.W., additional, Barnes, K.M., additional, Beale, E., additional, Beck, J.C., additional, Bennett, H.P.J., additional, Billard, R., additional, Blizzard, R.M., additional, Böhlen, P., additional, Borges, J.L.C., additional, Bradlow, H.L., additional, Brand, S.J., additional, Brandi, M.L., additional, Bremner, W.J., additional, Broadus, A.E., additional, Brook, C., additional, Burtis, W.J., additional, Callard, G., additional, Callard, I., additional, Campbell, G.T., additional, Campen, C., additional, Carey, R.M., additional, Caruso-Nicoletti, M., additional, Cassorla, F.G., additional, Catterall, J.F., additional, Chang, J.P., additional, Chen, T.T., additional, Clark, J.H., additional, Cohen, S., additional, Comite, F., additional, Cronin, M.J., additional, Cuello, C., additional, Cutler, G.B., additional, Delahunty, G., additional, Dobyns, B.M., additional, Draper, M.W., additional, Drucker, W.D., additional, Eckstein, B., additional, Esch, F., additional, Evans, W.S., additional, Everitt, B., additional, Feuillan, P., additional, Fitzpatrick, L.A., additional, Foster, C.M., additional, Foster, D.L., additional, Freeman, M.W., additional, Friesen, H.G., additional, Frohman, L., additional, Funkenstein, D., additional, Furlanetto, R., additional, Garcia, H.B., additional, Geller, J., additional, Gill, J.R., additional, Godsall, J.W., additional, Goldstein, M., additional, Goltzman, D., additional, Gorski, J., additional, Granner, D.K., additional, Greengard, P., additional, Greep, R., additional, Greer, M.A., additional, Grumbach, M.M., additional, Guillemin, R., additional, Hansen, J., additional, Hart, C., additional, Hemmings, H., additional, Hench, K.D., additional, Hershman, J.M., additional, Hickok, N.J., additional, Hinds, L.A., additional, Ho, K., additional, Hoffman, R.A., additional, Hökfelt, T., additional, Horton, T., additional, Horvath, E., additional, Hulting, A.-L., additional, Igarashi, T., additional, Insogna, K.L., additional, Jänne, O.A., additional, Johansson, O., additional, Kaplan, S.L., additional, Karch, F.J., additional, Kassis, J., additional, Katz, M.S., additional, Keefe, D.L., additional, Kelch, R.P., additional, Kelly, P.A., additional, Kelly, T.M., additional, Kenigsburg, D., additional, Klingensmith, G.J., additional, Knobil, E., additional, Kontula, K.K., additional, Koutsilieris, M., additional, Kovacs, K., additional, Kronenberg, H.M., additional, Kulin, H., additional, Laherty, R.F., additional, Lakoski, J.M., additional, Laue, L., additional, Lederis, K., additional, Lefevre, Y.A., additional, Leong, D.A., additional, LeRoith, D., additional, Lesniak, M.A., additional, Ling, N., additional, Long, L.M., additional, Loriaux, D.L., additional, Lundberg, J.M., additional, Maack, T., additional, MacDonald, G.J., additional, MacLeod, R.M., additional, McConnell, S.J., additional, Means, A., additional, Meister, B., additional, Melander, T., additional, Melanitou, E., additional, Meiner, M.H., additional, Meserve, L.A., additional, Mitchell, J., additional, Morgan, R.O., additional, Mormède, P., additional, Morris, D.J., additional, Murphy, L., additional, Nahorniak, C.S., additional, Nekola, M.V., additional, New, M.I., additional, Nicoll, C.S., additional, Nolin, J.M., additional, Odell, W.D., additional, Ojeda, S.R., additional, Okazaki, T., additional, Olster, D.H., additional, Omeljaniuk, R.J., additional, Osathanondh, R., additional, Ouimet, C., additional, Papkoff, H., additional, Pescovitz, O.H., additional, Peter, R.E., additional, Pomerantz, D.K., additional, Potts, J.T., additional, Rabbani, S.A., additional, Raj, M., additional, Rall, J.E., additional, Reichlin, S., additional, Rice, B.F., additional, Rittmaster, R., additional, Rivier, J., additional, Roberts, C.T., additional, Robinson, J., additional, Rogol, A.D., additional, Ross, J.L., additional, Roth, J., additional, Rouleau, M.F., additional, Ryan, K.D., additional, Ryan, R., additional, Saffran, M., additional, Sakai, D., additional, Samaan, N., additional, Sasaki, K., additional, Schalling, M., additional, Schriock, E.A., additional, Schwartz, N.B., additional, Scoggins, B.A., additional, Segre, G., additional, Sen, S., additional, Seppänen, P.J., additional, Shemer, J., additional, Sherman, M.R., additional, Shih, S.H., additional, Shiloach, J., additional, Shull, J., additional, Singh, P., additional, Skerda, M.C., additional, Smith, P., additional, Sokolowska, M., additional, Spitz, I.M., additional, Stack, G., additional, Stewart, A.F., additional, Stewart, D.R., additional, Tait, J.F., additional, Terasawa, E., additional, Thorner, M.O., additional, Tyndale-Biscoe, C.H., additional, Ueno, N., additional, Urbanski, H.F., additional, Uriarte, M., additional, Vale, W., additional, Vance, M.L., additional, VanderLaan, W., additional, Vecsei, P., additional, Veldhuis, J.D., additional, Walaas, I., additional, Walent, J., additional, Walters, M., additional, Watson, C.S., additional, Wehrenberg, W.B., additional, Welshons, W.V., additional, Werner, S., additional, Wilson, G.L., additional, Wiren, K.M., additional, Yellon, S.M., additional, Ying, S.-Y., additional, and Yoshinaga, K., additional

Published
1986
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30. Estimation of combat-related blood group alloimmunization and delayed serologic transfusion reactions in U.S. military veterans.

Author

Tormey CA, Stack G, Tormey, Christopher A, and Stack, Gary

Abstract

The goals of this study were to estimate blood group alloimmunization arising from combat-related transfusion and the prevalence of delayed serologic transfusion reactions (DSTRs) in military veteran patients. Blood group alloantibodies documented in the transfusion records at a Veterans Affairs (VA) medical center were categorized according to whether they developed before ("pre-existing") or during ("hospital-acquired") VA care and whether they were associated with anamnestic immune responses. Combat-related alloantibodies were estimated by adding anamnestic to pre-existing antibodies, revealing that 256 veterans made 322 combat-related alloantibodies. The combat-related alloimmunization rate was 1.37% (256/18,750), and combat-related alloantibodies represented 55.8% (322/577) of total alloantibodies. The highest rate of combat-related alloimmunization was observed in World War II-era veterans. Approximately 11.2% (25/224) of veterans with hospital-acquired antibodies experienced a DSTR due to prior alloimmunization. In conclusion, combat-related alloimmunization accounted for more than half of antibodies in military veterans and was a predisposing factor for DSTRs. [ABSTRACT FROM AUTHOR]

Published
2009
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33. Blood product replacement in the perinatal period.

Author

Wu Y and Stack G

Abstract

OBJECTIVE: In this article, we will describe some of the special compatibility testing procedures and blood component preparation and modification techniques used in intrauterine and neonatal transfusion medicine. We also will review the transfusion therapy used in hemolytic disease of the fetus and newborn (HDFN) and fetal and neonatal alloimmune thrombocytopenia (FNAIT). FINDING: Transfusion therapy in the fetus and neonate requires blood typing and compatibility testing techniques not routinely used for adults. These include: cord blood testing, special attention to the volume and speed of infusion, cytomegalovirus risk reduction, and routine irradiation of cellular blood components. The treatment of HDFN and FNAIT involves phenotyping and/or genotyping of fetal and paternal red blood cells and platelets. In FNAIT, platelet products are chosen based on the absence of platelet-specific antigens. CONCLUSION: Fetal and neonatal transfusion medicine require special attention to the unique anatomic and physiologic features of early human development. Copyright © 2007 by Elsevier Inc. [ABSTRACT FROM AUTHOR]

Published
2007

43. Neutrophils Recruited by IL-22 in Peripheral Tissues Function as TRAIL-Dependent Antiviral Effectors against MCMV

Author

Humphreys, I, Stacey, M, Marsden, M, Pham, T, Clare, S, Dolton, G, Stack, G, Jones, E, Klenerman, P, Gallimore, A, Taylor, P, Snelgrove, R, Lawley, T, Dougan, G, Benedict, C, Jones, SA, and Wilkinson, G

Subjects
Cancer Research, Immunology and Microbiology(all), Molecular Biology, R1
Abstract

SummaryDuring primary infection, murine cytomegalovirus (MCMV) spreads systemically, resulting in virus replication and pathology in multiple organs. This disseminated infection is ultimately controlled, but the underlying immune defense mechanisms are unclear. Investigating the role of the cytokine IL-22 in MCMV infection, we discovered an unanticipated function for neutrophils as potent antiviral effector cells that restrict viral replication and associated pathogenesis in peripheral organs. NK-, NKT-, and T cell-secreted IL-22 orchestrated antiviral neutrophil-mediated responses via induction in stromal nonhematopoietic tissue of the neutrophil-recruiting chemokine CXCL1. The antiviral effector properties of infiltrating neutrophils were directly linked to the expression of TNF-related apoptosis-inducing ligand (TRAIL). Our data identify a role for neutrophils in antiviral defense, and establish a functional link between IL-22 and the control of antiviral neutrophil responses that prevents pathogenic herpesvirus infection in peripheral organs.

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44. New Generation Dopaminergic Agents. 1. Discovery of a Novel Scaffold Which Embraces the D<INF>2</INF> Agonist Pharmacophore. Structure−Activity Relationships of a Series of 2-(Aminomethyl)chromans

Author

Mewshaw, R. E., Kavanagh, J., Stack, G., Marquis, K. L., Shi, X., Kagan, M. Z., Webb, M. B., Katz, A. H., Park, A., Kang, Y. H., Abou-Gharbia, M., Scerni, R., Wasik, T., Cortes-Burgos, L., Spangler, T., Brennan, J. A., Piesla, M., Mazandarani, H., Cockett, M. I., Ochalski, R., Coupet, J., and Andree, T. H.

Abstract

A series of 2-(aminomethyl)chromans (2-AMCs) was synthesized and evaluated for their affinity and selectivity for both the high- and low-affinity agonist states (D2High and D2Low, respectively) of the dopamine (DA) D2 receptor. The 7-hydroxy-2-(aminomethyl)chroman moiety was observed to be the primary D2 agonist pharmacophore. The 2-methylchroman moiety was discovered to be an entirely novel scaffold which could be used to access the D2 agonist pharmacophore. Attaching various simple alkyl and arylalkyl side chains to the 7-hydroxy 2-AMC nucleus had significant effects on selectivity for the D2High receptor vs the 5HT1A and α1 receptors. A novel DA partial agonist, (R)-(−)-2-(benzylamino)methyl)chroman-7-ol [R-(−)-35c], was identified as having the highest affinity and best selectivity for the D2High receptor vs the α1 and 5HT1A receptors. Several regions of the 2-AMC nucleus were modified and recognized as potential sites to modulate the level of intrinsic activity. The global minimum conformer of the 7-hydroxy-2-AMC moiety was identified as fulfilling the McDermed model D2 agonist pharmacophoric criteria and was proposed as the D2 receptor-bound conformation. Structure−activity relationships gained from these studies have aided in the synthesis of D2 partial agonists of varying intrinsic activity levels. These agents should be of therapeutic value in treating disorders resulting from hypo- and hyperdopaminergic activity, without the side effects associated with complete D2 agonism or antagonism.

Published
1997

46. The Effect of Annealing on the Thermal and Dynamic Mechanical Properties of TMXDI Based Polyurethanes

Author

NAVAL RESEARCH LAB ORLANDO FL UNDERWATER SOUND REFERENCE DETACHMENT, Stack, G. M., NAVAL RESEARCH LAB ORLANDO FL UNDERWATER SOUND REFERENCE DETACHMENT, and Stack, G. M.

Abstract

Reprint: The Effect of Annealing on the Thermal and Dynamic Mechanical Properties of TMXDI Based Polyurethanes., Availability: Pub. in Proceedings of the North American Thermal Analysis Society Conference (18th) p802-803, 24-27 Sep 1989.

Published
1989

47. Piezoelectric Properties and Temperature Stability of Poly (Vinylidene Fluoride-Trifluoroethylene) Copolymers.

Author

NAVAL RESEARCH LAB ORLANDO FLA UNDERWATER SOUND REFERENCE DIV, Stack, G M, Ting, R Y, NAVAL RESEARCH LAB ORLANDO FLA UNDERWATER SOUND REFERENCE DIV, Stack, G M, and Ting, R Y

Abstract

Piezoelectric measurements were made on several copolymers of vinylidene fluoride and trifluoroethylene having a vinylidene fluoride concentration in the range of 65 to 75%. The hydrostatic g constant showed only a slight dependence on pressure, and pressures up to 35 MPa caused no apparent loss of the piezoelectric activity. A significant increase in the value of the hydrostatic g constant occurred with an increase in temperature. Anomalous results obtained upon cooling below room temperature may be attributed to the glass transition temperature of the trifluoroethylene comonomer. Temperature aging studies were performed at high temperatures using films of these copolymers. A significant loss of piezoelectric activity occurred after long time exposure. Isothermal studies at various aging temperatures revealed that this decay continued over a long time span. The aging behaviour characteristically followed a linear dependence on the logarithm of aging time. Keywords: Piezoelectric measurements; Vinylidene fluoride copolymers; Temperature stability., Presented at the Proceedings of the IEEE International Symposium on Applications of Ferroelectrics (6th) Bethlehem, PA 8-11 June 1986.

Published
1986

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