Microbiology & Immunology - Research Publications
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ItemNo Preview AvailableQ&A: What do we know about influenza and what can we do about it?(Springer Science and Business Media LLC, 2009)
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ItemNo Preview AvailableThe challenge of viral immunity(CELL PRESS, 2007-09)Bringing together discussion of innate immunity, B cell and T cell responses, vaccine design and efficacy, and the genetics of HIV and AIDS resistance allows us to access the extraordinary complexity of viral immunity and host responsiveness.
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ItemCell-mediated protection in influenza infection(CENTERS DISEASE CONTROL & PREVENTION, 2006-01)Current vaccine strategies against influenza focus on generating robust antibody responses. Because of the high degree of antigenic drift among circulating influenza strains over the course of a year, vaccine strains must be reformulated specifically for each influenza season. The time delay from isolating the pandemic strain to large-scale vaccine production would be detrimental in a pandemic situation. A vaccine approach based on cell-mediated immunity that avoids some of these drawbacks is discussed here. Specifically, cell-mediated responses typically focus on peptides from internal influenza proteins, which are far less susceptible to antigenic variation. We review the literature on the role of CD4+ and CD8+ T cell-mediated immunity in influenza infection and the available data on the role of these responses in protection from highly pathogenic influenza infection. We discuss the advantages of developing a vaccine based on cell-mediated immune responses toward highly pathogenic influenza virus and potential problems arising from immune pressure.
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ItemNo Preview AvailableThe virus-immunity ecosystem(SPRINGER WIEN, 2005)The ecology of pathogenic viruses can be considered both in the context of survival in the macro-environments of nature, the theme pursued generally by epidemiologists, and in the micro-environments of the infected host. The long-lived, complex, higher vertebrates have evolved specialized, adaptive immune systems designed to minimise the consequences of such parasitism. Through evolutionary time, the differential selective pressures exerted variously by the need for virus and host survival have shaped both the "one-host" viruses and vertebrate immunity. With the development of vaccines to protect us from many of our most familiar parasites, the most dangerous pathogens threatening us now tend to be those "emerging", or adventitious, infectious agents that sporadically enter human populations from avian or other wild-life reservoirs. Such incursions must, of course, have been happening through the millenia, and are likely to have led to the extraordinary diversity of recognition molecules, the breadth in effector functions, and the persistent memory that distinguishes the vertebrate, adaptive immune system from the innate response mechanisms that operate more widely through animal biology. Both are important to contemporary humans and, particularly in the period immediately following infection, we still rely heavily on an immediate response capacity, elements of which are shared with much simpler, and more primitive organisms. Perhaps we will now move forward to develop useful therapies that exploit, or mimic, such responses. At this stage, however, most of our hopes for minimizing the threat posed by viruses still focus on the manipulation of the more precisely targeted, adaptive immune system.
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ItemCYTOTOXIC THYMUS-DERIVED LYMPHOCYTES IN CEREBROSPINAL-FLUID OF MICE WITH LYMPHOCYTIC CHORIOMENINGITIS(ROCKEFELLER UNIV PRESS, 1973)
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ItemH-2 COMPATIBILITY IS REQUIRED FOR T-CELL-MEDIATED LYSIS OF TARGET-CELLS INFECTED WITH LYMPHOCYTIC CHORIOMENINGITIS VIRUS(ROCKEFELLER UNIV PRESS, 1975)Maximal cell-mediated lysis of targets infected with lymphocytic choriomeningitis virus occurs only within a H-2 compatible system. Syngeneic immune spleen cells are at least 100 times as effective as are allogeneic lymphocytes. Reciprocal restriction of cytotoxic T-cell activity has been shown to operative between H-2k, H-2d, and H-2b. Experiments with cogenic mice have localized the effect to the H-2 gene complex. Furthermore, the observation that lymphocytes from H-2a mice cause high specific 51Cr release from either H-2d virus-infected cells, indicates that identity at either the K or the D end of the H-2 gene complex is sufficient for this lytic interaction.
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ItemCONTROL OF SPECIFICITY OF CYTOTOXIC T LYMPHOCYTES BY MAJOR HISTOCOMPATIBILITY COMPLEX (AG-B) IN RATS AND IDENTIFICATION OF A NEW ALLOANTIGEN SYSTEM SHOWING NO AG-B RESTRICTION(ROCKEFELLER UNIV PRESS, 1977)The regulatory influence of the rat major histocompatibility complex (MHC) (Ag-B complex) on the specificity of cytotoxic T lymphocytes was investigated. It was shown that the effector cells were specific for the original Ag-B phenotype in rat systems in which the responder and stimulator cell populations were unquestionably MHC identical but expressed different minor alloantigens of viral antigens. However, combined in vivo immunization and restimulation in culture of lymphocytes from rat strains previously thought to be MHC compatible resulted in the generation of cytotoxic T lymphocytes which effectively lyse not only target cells from the specific stimulating strains but also, to varying degrees, target cells from third party strains regardless of their Ag-B haplotypes. Genetic analysis indicates that expression of these cytotoxic T-cell-defined ("CT") antigens, found on both T and B lymphocytes, detectable thus far only with cytotoxic lymphocytes, is controlled by a single locus which segregates in backcross populations with the rat MHC. Discrepancies between the nature of CT antigens of the rat Ag-B and I-region specificities of the mouse H-2 are discussed.
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ItemINHIBITION OF AUTOIMMUNE NEUROPATHOLOGICAL PROCESS BY TREATMENT WITH AN IRON-CHELATING AGENT(ROCKEFELLER UNIV PRESS, 1984)Lewis rats that are primed with guinea pig spinal cord homogenized in complete Freund's adjuvant (GPSCH-CFA) develop overt symptoms of experimental allergic encephalomyelitis (EAE). Treatment with the iron-chelating agent, desferrioxamine B mesylate (DFOM), at various times before the onset of EAE, dramatically suppressed both the severity and duration of disease. When DFOM was administered to rats soon after the development of neurological signs, a rapid recovery occurred, though mild, transient symptoms could be seen approximately 1 wk after withdrawal of the drug. Treatment with DFOM was always accompanied by a diminution of T cell responsiveness on the part of the delayed-type hypersensitivity/helper subset and, on histological examination, an absence of inflammatory cells from lesions. Iron is believed to influence both the migration and function of immune effector cells. It can also act as a catalyst in the formation of free radicals, which are highly toxic agents causing tissue damage in sites of inflammation. The mechanisms underlying the effect of DFOM on the severity of EAE, and the possible implications for treatment of multiple sclerosis are discussed.
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ItemACTIVATION OF CYTOKINE GENES IN T-CELLS DURING PRIMARY AND SECONDARY MURINE INFLUENZA PNEUMONIA(ROCKEFELLER UNIV PRESS, 1993-02-01)The patterns of cytokine mRNA expression in mice with primary or secondary influenza pneumonia have been assessed by in situ hybridization analysis of cells from both the mediastinal lymph node (MLN) and the virus-infected lung. Evidence of substantial transcriptional activity was found in all lymphocyte subsets recovered from both anatomical sites. The kinetics of cytokine mRNA expression after primary infection with an H3N2 virus were in accord with the idea that the initial response occurs in regional lymphoid tissue, with the effector T cells later moving to the lung. This temporal separation was much less apparent for the more rapid secondary response resulting from challenge of H3N2-primed mice with an H1N1 virus. Among the T cell receptor alpha/beta+ subsets, transcripts for interferon (IFN) gamma and tumor necrosis factor beta were most commonly found in the CD8+ population whereas mRNA for interleukin (IL) 4 and IL-10 was much more prevalent in CD4+ T cells. The gamma/delta T cells expressed mRNA for all cytokines tested, with IL-2, IL-4, and IFN-gamma predominating among those recovered from the inflammatory exudate. At particular time points, especially early in the MLN and late in the infected lung, the frequency of mRNA+ lymphocytes was much higher than would be expected from current understanding of the prevalence of virus-specific precursors and effectors. If this response is typical, induction of cytokine gene expression for T cells that are not responding directly to the invading pathogen may be a prominent feature of acute virus infections.