Justin D Radolf
University Of Connecticut Sch Of Med/dnt
Project start date: 1992-07-01
Project end date: 2012-12-31
Sponsored Links Excellgen http://Excellgen.com
MEMBRANE IMMUNOGENS OF TREPONEMA PALLIDUM
Justin D Radolf, Director/ Professor
University Of Connecticut Sch Of Med/dnt 263 Farmington Avenue Farmington, Ct 060302806
Grant 5R01AI026756-14 from National Institute Of Allergy And Infectious Diseases IRG: ZRG5
Abstract: From combined biochemical, ultrastructural and molecular studies conducted during the PI s FIRST AWARD, a novel model has emerged from the molecular architecture of Treponema pallidum, the etiologic agent of venereal syphilis. According to this new model, the T. pallidum outer membrane contains a rare transmembrane protein, tentatively identified as a 32-Kda polypeptide, while the major membrane immunogens (formerly thought to be located in the outer membrane) are integral cytoplasmic membrane proteins. To accommodate the newly discovered lipoprotein structures of the major membrane immunogens, the model further proposes that these immunogens comprise a "family" of hydrophilic polypeptides located within the periplasmic space and anchored to the external leaflet of the cytoplasmic membrane via lipids bound to their N-terminal cysteine residues. Furthermore, we have identified potent immunostimulatory properties of these membrane immunogens (cytokine production and Ia expression by macrophages), which may derive from their lipoprotein structures. The research in this proposal will refine the above model and delineate the structural and biochemical requirements for macrophage activation by the lipoproteins. First, we will confirm that the 32-Kda protein in isolated outer membrane preparations is a rare outer membrane protein of T. pallidum (Specific Aim I). This will be accomplished by raising murine monoclonal antibodies against the rare protein and demonstrating, by a variety of techniques, including freeze-fracture cytochemistry, that they react with the surface of intact T. pallidum. Second, we will confirm the membrane topologies predicted for the lipoprotein immunogens by analyzing the native lipoproteins in T. pallidum, the cloned immunogens expressed in E. coli, and the purified lipoproteins reconstituted into liposomes (Specific Aim II). Lastly, we will characterize further the immunological properties of the lipoproteins and determine the structural features of these molecules (e.g. the covalently bound lipids) which contribution to their immunostimulatory activities (Specific Aim III). The ultimate strength of this proposal is that it presents the first coherent model for T. pallidum ultrastructure that accounts for the remarkable immunological evasiveness of the pathogen and the intense immunological phenomena which characterize human syphilis.
Keywords: Treponema pallidum, bacterial antigen, bacterial protein, membrane protein, protein structure /function, ampicillin, cardenolide, glycolipid, laboratory rabbit
Project start date: 1992-07-01
Project end date: 2002-06-30
5R01AI026756-14 (2000): $319498
5R01AI026756-13 (1999): $307255
5R01AI026756-11 (1998): $318372
5R01AI026756-10 (1997): $308282
5R01AI026756-08 (1995): $256692
5R01AI026756-07 (1994): $269072
5R01AI026756-06 (1993): $258506
TREPONEMA PALLIDUM OUTER MEMBRANE PROTEINS AND TRANSITION METAL ACQUISITION
Justin D Radolf, Professor
University Of Connecticut Sch Of Med/dnt, Office Of Research & Sponsored Programs, Farmington, Ct 06030
Grant 5R01AI026756-22 from National Institute Of Allergy And Infectious Diseases
Keywords: Animal Welfare; Bibliography; Country; Ecological impact; Environment; Environmental Impact; Equipment; Ethics Committees, Research; IACUC; IRBs; Impact, Environmental; Institutional Animal Care and Use Committee; Institutional Review Boards; International; Membrane Proteins; Membrane-Associated Proteins; Names; Principal Investigator; Programs (PT); Programs [Publication Type]; Research; Research Ethics Committees; Research Resources; Resources; Stream; Surface Proteins; T. pallidum; T.pallidum; Transition Elements; Treponema pallidum; Vertebrate Animals; Vertebrates; ing; expiration; human subject; programs; transition metal; vertebrata
Project start date: 1992-07-01
Project end date: 2012-12-31
Budget start date: 1-JAN-2010
Budget end date: 31-DEC-2010
PFA/PA: PA-07-070
5R01AI026756-22 (2010): $443005
Grants awarded to Justin D Radolf
Cutaneous Immune Response In Lyme Disease And Secondary Syphilis
Justin D Radolf, Director/ Professor
University Of Connecticut Sch Of Med/dnt 263 Farmington Avenue Farmington, Ct 060302806
Grant 5M01RR006192-070186 from National Center For Research Resources IRG: RIRG
Abstract: Venereal syphilis is a chronic inflammatory disorder driven by the persistence of its etiologic agent Treponema pallidum. Though the immune/inflammatory response at sites of local treponemal infection may ultimately underlie the development of both protective immunity and clinical manifestations, these local cellular processes have yet to be characterized in humans using the tools of contemporary cellular and molecular immunology. The components of T. pallidum that induce these potentially deleterious inflammatory processes also remain poorly characterized. Our understanding of cellular immunity in syphilis is further compromised by our currently limited knowledge concerning the interactions between syphilis and HIV infection. Accordingly, the proposed research has three Specific Aims. In Specific Aim 1, we will perform immunocytochemical analysis of skin biopsies and flow cytometry analysis of leukocytes in suction blisters to characterize cutaneous cellular immune processes in HIV- and HIV+ patients with secondary syphilis. Data from these studies will be correlated with our in vitro research involving immune effector cell activation by T. pallidum and treponemal lipoproteins. In Specific Aim 2, we will use the same immunocytochemical and flow cytometric approaches to characterize the cutaneous inflammatory response to synthetic analogs (lipopeptides) of T. pallidum lipoproteins. These experiments are an outgrowth of our hypothesis that T. pallidum lipoproteins are major inflammatory mediators during syphilitic infection. Building upon our observation that T. pallidum lipoprotein analogs induce HIV gene expression in vitro, the experiments in Specific Aim 3 will elucidate the mechanisms which underlie this phenomenon. A principal long-term objective of this research is to elucidate the immune/inflammatory events during syphilitic infection which engender both clinical manifestations and protective immunity. An equally important objective is to obtain cellular and molecular data which will complement our emerging understanding of the interactions between syphilis and HIV infection, including the potential for syphilis to serve as a co-factor for HIV transmission and for HIV infection to alter the clinical course of syphilis.
Keywords: HIV infection, cellular immunity, comorbidity, inflammation, pathologic process, syphilis, Treponema pallidum, bacterial cytopathogenic effect, bacterial protein, gene expression, host organism interaction, leukocyte, nonblood lipoprotein, biopsy, clinical research, flow cytometry, human subject, immunocytochemistry
Project start date: 1993-12-15
Project end date: 2003-11-30
CUTANEOUS IMMUNE RESPONSE IN SECONDARY SYPHILIS
Justin D Radolf, Director/ Professor
University Of Connecticut Sch Of Med/dnt 263 Farmington Avenue Farmington, Ct 060302806
Grant 5R01AI038894-05 from National Institute Of Allergy And Infectious Diseases IRG: ZRG5
Abstract: Venereal syphilis is a chronic inflammatory disorder driven by the persistence of its etiologic agent Treponema pallidum. Though the immune/inflammatory response at sites of local treponemal infection may ultimately underlie the development of both protective immunity aid clinical manifestations, these local cellular processes have yet to be characterized in humans using the tools of contemporary cellular and molecular immunology. The components of T. pallidum that induce these potentially deleterious inflammatory processes also remain poorly characterized. Our understanding of cellular immunity in syphilis is further compromised by our currently limited knowledge concerning the interactions between syphilis and HIV infection. Accordingly, the proposed research has three Specific Aims. In Specific Aim 1, we will perform immunocytochemical analysis of skin biopsies and flow cytometry analysis of leukocytes in suction blisters to characterize cutaneous cellular immune processes in HIV- and HIV+ patients with secondary syphilis. Data from these studies will be correlated with our in vitro research involving immune effector cell activation by T. pallidum and treponemal lipoproteins. In Specific Aim 2, we will use the same immunocytochemical and flow cytometric approaches to characterize the cutaneous inflammatory response to synthetic analogs (lipopeptides) of T pallidum lipoproteins. These experiments are an outgrowth of our hypothesis that T. pallidum lipoproteins are major inflammatory mediators during syphilitic infection. Building upon our observation that T pallidum lipoprotein analogs induce HIV gene expression in vitro, the experiments in Specific Aim 3 will elucidate the mechanisms which underlie this phenomenon. A principal long-term objective of this research is to elucidate the immune/inflammatory events during syphilitic infection which engender both clinical manifestations and protective immunity. An equally important objective is to obtain cellular and molecular data which will complement our emerging understanding of the interactions between syphilis and HIV infection, including the potential for syphilis to serve as a co-factor for HIV transmission and for HIV infection to alter the clinical course of syphilis.
Keywords: HIV infection, cellular immunity, secondary infection, skin hypersensitivity, syphilis, Treponema pallidum, bacterial protein, blister, cofactor, communicable disease transmission, human immunodeficiency virus, immunomodulator, leukocyte activation /transformation, peptide analog, synthetic peptide, CD antigen, biopsy, clinical research, flow cytometry, human subject, immunocytochemistry, laboratory rabbit
Project start date: 1996-04-01
Project end date: 2001-03-31
5R01AI038894-05 (2000): $266349
5R01AI038894-03 (1998): $248073
5R01AI038894-02 (1997): $234839
MEMBRANE IMMUNOGENS OF TREPONEMA PALLIDUM
Justin D Radolf, Director/ Professor
University Of Texas Sw Med Ctr/dallas Dallas, Tx 753909105
Grant 2R01AI026756-05 from National Institute Of Allergy And Infectious Diseases IRG: BM
Abstract: From combined biochemical, ultrastructural and molecular studies conducted during the PI s FIRST AWARD, a novel model has emerged from the molecular architecture of Treponema pallidum, the etiologic agent of venereal syphilis. According to this new model, the T. pallidum outer membrane contains a rare transmembrane protein, tentatively identified as a 32-Kda polypeptide, while the major membrane immunogens (formerly thought to be located in the outer membrane) are integral cytoplasmic membrane proteins. To accommodate the newly discovered lipoprotein structures of the major membrane immunogens, the model further proposes that these immunogens comprise a "family" of hydrophilic polypeptides located within the periplasmic space and anchored to the external leaflet of the cytoplasmic membrane via lipids bound to their N-terminal cysteine residues. Furthermore, we have identified potent immunostimulatory properties of these membrane immunogens (cytokine production and Ia expression by macrophages), which may derive from their lipoprotein structures. The research in this proposal will refine the above model and delineate the structural and biochemical requirements for macrophage activation by the lipoproteins. First, we will confirm that the 32-Kda protein in isolated outer membrane preparations is a rare outer membrane protein of T. pallidum (Specific Aim I). This will be accomplished by raising murine monoclonal antibodies against the rare protein and demonstrating, by a variety of techniques, including freeze-fracture cytochemistry, that they react with the surface of intact T. pallidum. Second, we will confirm the membrane topologies predicted for the lipoprotein immunogens by analyzing the native lipoproteins in T. pallidum, the cloned immunogens expressed in E. coli, and the purified lipoproteins reconstituted into liposomes (Specific Aim II). Lastly, we will characterize further the immunological properties of the lipoproteins and determine the structural features of these molecules (e.g. the covalently bound lipids) which contribution to their immunostimulatory activities (Specific Aim III). The ultimate strength of this proposal is that it presents the first coherent model for T. pallidum ultrastructure that accounts for the remarkable immunological evasiveness of the pathogen and the intense immunological phenomena which characterize human syphilis.
Keywords: Treponema pallidum, bacterial antigen, bacterial protein, bactericidal immunity, leukocyte activation /transformation, macrophage, membrane protein, syphilis, liposome, membrane reconstitution /synthesis, protein structure, Escherichia coli, electron microscopy, human tissue, laboratory rabbit, molecular cloning, monoclonal antibody
Project start date: 1992-07-01
Project end date: 1996-06-30
2R01AI026756-05 (1992): $218864
RPOS REGULATION OF BORRELIA BURGDORFERI GENES IN VIVO
Justin D Radolf, Professor
University Of Connecticut Sch Of Med/dnt, Office Of Research & Sponsored Programs, Farmington, Ct 06030
Grant 5R01AI029735-20 from National Institute Of Allergy And Infectious Diseases
Abstract: Borrelia burgdorferi (Bb), the Lyme disease (LD) spirochete, is maintained in nature via an enzootic cycle which typically involves wild rodents and Ixodes ticks. During the current funding interval, we have used an expanding armamentarium of model systems and genetic tools to define the physiological and virulence-related functions of Bb genes involved in mammalian host adaptation as well as the mechanisms that underlie the spirochete´s transition from arthropod vector to mammalian host. Much of this work has centered about delineating the relative contributions of the RpoS-dependent and -independent transcriptional pathways to the processes which enable spirochetes to transit from tick to mammal. Microarray-based transcriptional profiling of wild-type and rpoS mutant spirochetes grown in dialysis membrane chambers (DMCs) has enabled us to define the in vivo RpoS regulon, the cohort of genes that the alternate sigma factor RpoS controls, both positively and negatively, in response to mammalian host-derived signals. By extrapolating from these and related findings to the scenario of the infected nymphal tick, we have formulated our central hypothesis beginning with the taking of the blood meal, RpoS acts as a "gatekeeper" that coordinates the reciprocal upregulation and repression of a subset of differentially expressed borrelial genes required to establish mammalian infection. As a corollary to this hypothesis, we propose that the "RpoS off´ state represents an alternate developmental program required by the spirochete to establish the tick-phase of the enzootic life cycle. The principal long-term objective of our Research Plan is to integrate the search for novel Bb virulence determinants that function within the tick or the mouse with efforts to decipher the mechanisms that underlie differential gene expression by the LD spirochete. To accomplish this objective, we have formulated three Specific Aims (i) to further characterize genes within the in vivo RpoS regulon which we hypothesize are induced by the blood meal and promote infection of the mammalian host; (ii) to further characterize genes which require RpoS for repression in vivo and which we hypothesize are required for the tick- phase of the spirochete´s life cycle; and (iii) to develop a broader understanding of the RpoS regulon by delineating its "on" and "off" states during the enzootic cycle and examining selected facets of RpoS function
Keywords: Arthropod Vectors; Arthropoda; Arthropods; B. burgdorferi; B.burgdorferi; Bacteria; Bacteria sigma factor KatF protein; Biological Models; Blood; Borrelia; Borrelia burgdorferi; Borrelia burgdorferi sensu stricto; Cell Communication and Signaling; Cell Signaling; Cues; Development; Dialysis; Dialysis procedure; Differential Gene Expression; Funding; Gatekeeping; Genes; Genetic; Infection; Intracellular Communication and Signaling; Ixodes; Ixodes (genus); Ixodes tick; Ixodida; KatF protein, Bacteria; Life Cycle; Life Cycle Stages; Lyme Borreliosis; Lyme Disease; Lyme Disease Spirochete; Mammalia; Mammals; Mammals, General; Mammals, Mice; Mammals, Rodents; Membrane; Mice; Model System; Models, Biologic; Murine; Mus; Nature; Order Spirochaetales; Pathway interactions; Phase; Physiologic; Physiological; Process; Programs (PT); Programs [Publication Type]; Regulation; Regulon; Relative; Relative (related person); Repression; Research; Reticuloendothelial System, Blood; Rodent; Rodentia; Rodentias; RpoS; Sigma Element; Sigma Factor; Sigma Initiation Factor; Sigma Subunit; Signal Transduction; Signal Transduction Systems; Signaling; Spirochaetales; Spirochetes; Ticks; Tissue-Specific Differential Gene Expression; Tissue-Specific Gene Expression; Up-Regulation; Up-Regulation (Physiology); Upregulation; Virulence; Virulent; Work; base; biological signal transduction; borrelial; cohort; dialysis therapy; enzootic; gatekeeper; in vivo; life course; lyme spirochete; membrane structure; mutant; novel; pathway; programs; response; rpoS protein, Bacteria; sigma factor 38 protein, Bacteria; sigma factor KatF protein, Bacteria; sigma factor S protein, Bacteria; sigma(38) protein, Bacteria; sigma(S) protein, Bacteria; tool
Project start date: 1990-04-01
Project end date: 2012-03-31
Budget start date: 1-APR-2010
Budget end date: 31-MAR-2011
5R01AI029735-20 (2010): $550715
3R01AI029735-20S1 (2010): $242167
5R01AI029735-19 (2009): $542241
2R01AI029735-17 (2007): $523541
Cutaneous Immune Response In Early Syphilis
Justin D Radolf, Director/ Professor
University Of Connecticut Sch Of Med/dnt 263 Farmington Avenue Farmington, Ct 060302806
Grant 5R01AI038894-10 from National Institute Of Allergy And Infectious Diseases IRG: BM
Abstract: Applicant s ) Venereal syphilis is a chronic inflammatory disorder driven by the persistence of its etiologic agent Treponema pallidum. Research in this proposal is based on the premise that the local (i.e., tissue-based) cellular immune responses to T. pallidum have two distinct, yet interrelated, consequences of fundamental importance to syphilis pathogenesis. They cause the tissue damage which ultimately gives rise to clinical manifestations, and they are primarily responsible for the clearance of bacteria, a prerequisite for lesion resolution. Human skin is the primary focus of our efforts to elucidate these processes because (a) it is the major target organ of early syphilitic infection, (b) it is easily accessible to in vivo experimentation, and (c) there exists a wealth of reagents and information concerning its immune-related functions. During the prior funding interval, we have made considerable progress in characterizing the cellular infiltrates in secondary syphilis lesions and in delineating the ontogeny of the cutaneous response engendered by the syphilis spirochete. A unifying theme of this work has been the acquisition of considerable evidence, using a combination of in vitro and in vivo approaches, to support our primary hypothesis that the proinflammatory properties of treponemal lipoproteins are the primary triggers of innate immune mechanisms in early syphilis. More recently, we have shown that by recruiting a cellular infiltrate rich in antigen presenting cells, particularly dendritic cells, and memory/effector T cells, the innate immune processes induced by these lipid-modified polypeptides set the stage for the adaptive (i.e., specific) immune responses to the bacterium. One important outcome of these findings is the recognition that the cutaneous responses under investigation relate to primary as well as to secondary syphilis. In this competitive renewal application, we will extend this conceptual framework by further characterizing the in vivo biological responses to treponemal lipoproteins/lipopeptides (Aim One); by further characterizing the cutaneous immune response to T pallidum in secondary syphilis lesions (Aim Two); by using in vitro/ex vivo approaches to examine dendritic and T cell responses to T pallidum and treponemal proteins (Aim Three); and by examining our hypothesis that treponemal lipoproteins activate macrophages following uptake and degradation within the phagosomal vacuoles of macrophages (Aim Four). This work will result in an enhanced appreciation of the role of local cellular responses in syphilis pathogenesis and will provide a necessary underpinning for the eventual development of a safe and effective syphilis vaccine.
Keywords: HIV infection, cellular immunity, immunopathology, secondary infection, skin hypersensitivity, syphilis, Treponema pallidum, bacterial protein, blister, cell cell interaction, cofactor, communicable disease transmission, human immunodeficiency virus, immunomodulator, leukocyte activation /transformation, macrophage, phagocytosis, biopsy, clinical research, human subject, immunocytochemistry
Project start date: 1996-04-01
Project end date: 2008-05-31
5R01AI038894-10 (2005): $384588
Sponsored Links Excellgen http://Excellgen.com
5R01AI038894-09 (2004): $373421
5R01AI038894-08 (2003): $362577
5R01AI038894-07 (2002): $351873
2R01AI038894-06 (2001): $311470
T.pallidum Membrane Immunogens And Anti-Oxidant Defense
Justin D Radolf, Director/ Professor
University Of Connecticut Sch Of Med/dnt 263 Farmington Avenue Farmington, Ct 060302806
Grant 5R37AI026756-19 from National Institute Of Allergy And Infectious Diseases IRG: BM
Abstract: Although much has been learned about venereal syphilis in the nearly one hundred years since the discovery of its etiologic agent, Treponema pallidum subsp. pallidum, the disease remains highly enigmatic. Our limited understanding of this chronic, systemic, sexually transmitted infection reflects the many peculiarities of the syphilis spirochete, which include the fragility and unusual molecular architecture of its outer membrane, an extremely narrow mammalian host range, and its inability to replicate continuously in artificial medium. A central theme of our research program has been and will continue to be the identification and characterization of rare outer membrane proteins. There are two principal reasons why we believe that this arduous search is about to reach a successful conclusion. First, using a lipophilic photoactivatable probe, we have identified what appears to be an authentic rare outer membrane protein, designate p30.5. Second, we now have at our disposal the T. pallidum genomic sequence, an extremely powerful too which now enables us to survey in silico the entire treponemal chromosome for additional candidate outer membrane proteins. Equally important, the T. pallidum genomic sequence has provided an invaluable platform for our investigations of physiological processes (i.e., trace metal acquisition and resistance to oxidative stress) which are fundamental to host- pathogen relations during syphilitic infection. Though clearly departures from our traditional areas of concentration, these new avenues of investigation are, nonetheless, outgrowths of our longstanding commitment to delineating in molecular terms the interface between the spirochete and its obligate human host. During the current funding interval, we have made substantial progress towards our long term objective of relating T. pallidum membrane biology to syphilis pathogenesis. In the present proposal, we hope to extend this process by integrating molecular, ultrastructural, and physiological information into a more complete picture of how the parasite sustains itself within the hostile host milieu. To achieve this end, we will molecularly characterize T. pallidum rare outer membrane proteins (Specific Aim One); define the roles of the Tro and TP0034 transporters in trace metal acquisition by T. pallidum (Specific Aim Two); and characterize key components of T. pallidum s defense against oxidative stress (Specific Aim Three).
Keywords: Treponema pallidum, antioxidant, bacterial antigen, bacterial protein, communicable disease transmission, membrane protein, oxidative stress, protein structure function, syphilis, gene expression, metal, oxidizing agent, pathologic process, trace element, laboratory rat
Project start date: 1992-07-01
Project end date: 2007-12-31
5R37AI026756-19 (2006): $353981
5R37AI026756-18 (2005): $362500
5R37AI026756-17 (2004): $362500
5R37AI026756-16 (2003): $362500
2R37AI026756-15 (2002): $362500
MEMBRANE PROTEINS OF BORRELIA BURGDORFERI
Justin D Radolf, Director/ Professor
University Of Connecticut Sch Of Med/dnt 263 Farmington Avenue Farmington, Ct 060302806
Grant 5R01AI029735-11 from National Institute Of Allergy And Infectious Diseases IRG: ZRG5
Abstract: Adapted from applicant s ) Over the past decade, numerous Borrelia burgdorferi proteins have been cloned and sequenced, while clinical and animal studies have delineated the basic microbiological events of Lyme disease. In contrast, we have a comparatively poor understanding of B. burgdorferi membrane biology and how general features of borrelial membrane architecture facilitate immune evasion during infection. Based upon extensive data obtained during the current funding period, the investigators have developed a new model of B. burgdorferi molecular architecture which helps to explain the bacterium s remarkable "immunoevasiveness". According to this model (1) the B. burgdorferi outer membrane contains uncharacterized poorly immunogenic membrane proteins in addition to well characterized outer surface lipoproteins, (2) the preponderance of outer surface proteins (Osps) A and B is sequestered within the periplasmic space (and therefore unavailable as targets for borreliacidal antibody), and (3) novel membrane proteins may be expressed during infection. Their first two Specific Aims describe two complimentary approaches for the molecular characterization of novel borrelial outer membrane proteins. The first is based upon a recently developed procedure for isolating B. burgdorferi outer membranes, while the second identifies candidate outer membrane proteins whose export signals are fused with an E. coli alkaline phosphatase (PhoA) reporter. Studies in Specific Aim 1 will be expedited by the fact that three conserved B. burgdorferi outer membrane proteins already have been identified in isolated outer membranes. Specific Aim 2 also includes detailed studies of three novel candidate outer membrane proteins, including an OspF homologue (designated BbK2.10) which is expressed only in vivo and which appears to be a member of a lipoprotein family. Experiments in our third Specific Aim will explore key ramifications of our findings that only small amounts of OspA and OspB are surface-exposed. Taken as a whole, these Specific Aims encompass our long term goal which is to integrate studies of B. burgdorferi membrane biology, Lyme disease pathogenesis, and vaccine development.
Keywords: Borrelia, Lyme disease, bacterial antigen, bacterial protein, membrane protein, alkaline phosphatase, fusion gene, microorganism immunology, nonblood lipoprotein, open reading frame, protein structure, reporter gene, Escherichia coli, confocal scanning microscopy, laboratory rat, nucleic acid hybridization
Project start date: 1990-04-01
Project end date: 2001-12-09
5R01AI029735-11 (2000): $369350
Sponsored Links Excellgen http://Excellgen.com
7R01AI029735-10 (1999): $355148
3R01AI029735-10S1 (1999): $156000
5R01AI029735-08 (1998): $341488
5R01AI029735-07 (1997): $359798
5R01AI029735-16 (2006): $427441
5R01AI029735-15 (2005): $426734
5R01AI029735-14 (2004): $416060
5R01AI029735-13 (2003): $405696
2R01AI029735-12 (2002): $394041
Cutaneous Immune Response In Lyme Disease And Secondary Syphilis
Justin D Radolf, Director/ Professor
University Of Connecticut Sch Of Med/dnt 263 Farmington Avenue Farmington, Ct 060302806
Grant 2M01RR006192-110186 from National Center For Research Resources IRG: RIRG
Keywords: HIV infection, Lyme disease, cellular immunity, comorbidity, immune response, inflammation, pathologic process, syphilis, Treponema pallidum, bacterial cytopathogenic effect, bacterial protein, gene expression, host organism interaction, leukocyte, nonblood lipoprotein, biopsy, clinical research, flow cytometry, human subject, immunocytochemistry
Project start date: 2004-04-15
Project end date: 2005-03-31
Sponsored Links Excellgen http://Excellgen.com
MEMBRANE IMMUNOGENS OF TREPONEMA PALLIDUM
Justin D Radolf, Director/ Professor
Internal Medicineuniversity Of Texas Sw Med Ctr/dallas
dallas, Tx 753909105
Grant 2R01AI026756-09 from National Institute Of Allergy And Infectious Diseases IRG: ZRG5
Project start date: 1992-07-01
Project end date: 2001-06-30
2R01AI026756-09 (1996): $397326
MEMBRANE PROTEINS OF BORRELIA BURGDORFERI
Justin D Radolf, Director/ Professor
Internal Medicineuniversity Of Texas Sw Med Ctr/dallas
dallas, Tx 753909105
Grant 3R01AI029735-06A1S1 from National Institute Of Allergy And Infectious Diseases IRG: ZRG5
Project start date: 1990-04-01
Project end date: 2001-01-31
3R01AI029735-06A1S1 (1996): $72608
CUTANEOUS IMMUNE RESPONSE IN SECONDARY SYPHILIS
Justin D Radolf, Director/ Professor
Internal Medicineuniversity Of Texas Sw Med Ctr/dallas
dallas, Tx 753909105
Grant 1R01AI038894-01 from National Institute Of Allergy And Infectious Diseases IRG: ZRG5
Project start date: 1996-04-01
Project end date: 2001-03-31
1R01AI038894-01 (1996): $214684
MEMBRANE PROTEINS OF BORRELIA BURGDORFERI
Justin D Radolf, Director/ Professor
Internal Medicineuniversity Of Texas Sw Med Ctr/dallas
dallas, Tx 753909105
Grant 2R01AI029735-06A1 from National Institute Of Allergy And Infectious Diseases IRG: ZRG5
Project start date: 1990-04-01
Project end date: 2001-01-31
2R01AI029735-06A1 (1996): $315726
MEMBRANE IMMUNOGENS OF TREPONEMA PALLIDUM
Justin D Radolf, Director/ Professor
University Of Texas Sw Med Ctr/dallas
dallas, Tx 753909105
Grant 3R01AI026756-05S1 from National Institute Of Allergy And Infectious Diseases IRG: BM
Project start date: 1992-07-01
Project end date: 1996-06-30
3R01AI026756-05S1 (1993): $13242