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Toll-Like Receptor Triggering of a Vitamin D-Mediated Human Antimicrobial Response
The data support a link between TLRs and vitamin D–mediated innate immunity and suggest that differences in ability of human populations to produce vitamin D may contribute to susceptibility to microbial infection.
Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors.
It is shown that microbial lipoproteins are potent stimulators of IL-12 production by human macrophages, and that induction is mediated by Toll-like receptors (TLRs), and that Activation of TLRs by microbes may initiate innate defense mechanisms against infectious pathogens.
New use of BCG for recombinant vaccines
Extrachromosomal and integrative expression vectors carrying the regulatory sequences for major BCG heat-shock proteins have been developed and can elicit long-lasting humoral and cellular immune responses to foreign antigens in mice.
An essential role for interferon gamma in resistance to Mycobacterium tuberculosis infection
- J. Flynn, J. Chan, K. Triebold, D. Dalton, T. Stewart, B. Bloom
- Biology, MedicineThe Journal of experimental medicine
- 1 December 1993
Gko mice have been developed which fail to produce IFN-gamma (gko), because of a targeted disruption of the gene for IFNs, and succumb to a rapid and fatal course of tuberculosis that could be delayed, but not prevented, by treatment with exogenous recombinant IFN.
Tumor necrosis factor-alpha is required in the protective immune response against Mycobacterium tuberculosis in mice.
Mutually dependent secretion of proteins required for mycobacterial virulence.
The results indicate that secretion of these proteins, which are each critical for virulence of pathogenic mycobacteria, is mutually dependent and suggest that discerning the nature of the interaction and the structure of macromolecular complexes will provide insights into both an alternative mechanism of protein secretion andMycobacterial virulence.
Tuberculosis: Commentary on a Reemergent Killer
The economic costs of not adequately addressing the problem of tuberculosis in this country are estimated from an epidemiological model.
Genome-wide requirements for Mycobacterium tuberculosis adaptation and survival in macrophages.
The majority of Mycobacterium tuberculosis genes found by this analysis to be required for survival are constitutively expressed rather than regulated by macrophages, revealing the host-adapted lifestyle of an evolutionarily selected intracellular pathogen.
An antimicrobial activity of cytolytic T cells mediated by granulysin.
The ability of CTLs to kill intracellular M. tuberculosis was dependent on the presence of granulysin in cytotoxic granules, defining a mechanism by which T cells directly contribute to immunity against intrACEllular pathogens.
Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages
The results from this study provide support for the view that the L-arginine-dependent production of RNI is the principal effector mechanism in activated murine macrophages responsible for killing and growth inhibiting virulent M. tuberculosis.