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Find video protocols related to scientific articles indexed in Pubmed.
Immunological hallmarks of JC virus replication in multiple sclerosis patients on long-term natalizumab therapy.
J. Virol.
PUBLISHED: 03-20-2013
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Progressive multifocal leukoencephalopathy (PML) is the main adverse effect of natalizumab. Detectable JC virus-specific effector memory T-cell (TEM) responses may indicate ongoing JCV replication. We detected JCV-specific TEM responses in blood of patients with multiple sclerosis (MS) treated with natalizumab, including 2 patients with PML. The frequency of detection of these responses increased with the time on natalizumab. Thus, a subset of MS patients exhibit immunological hallmarks of JCV replication during prolonged natalizumab therapy.
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Tissue Competence Imprinting and Tissue Residency of CD8 T Cells.
Front Immunol
PUBLISHED: 01-01-2013
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T cell immunity is characterized by striking tissue specialization. Tissue-specificity imprinting starts during priming by tissue-derived migratory dendritic cells in the non-random, specialized micro-anatomical area of the draining lymph node and is influenced by constitutive and induced cues from local environment. Besides tissue-specific effectors, memory cells also exhibit a tissue-specificity. Long-lived tissue-resident memory T cells likely play a considerable role in preventing pathogen invasion. Understanding of the mechanisms of tissue specialization of T cells is of major importance for the design of optimal vaccination strategies and therapeutic interventions in tissue/organ-specific inflammatory diseases. The present review summarizes our current knowledge and hypothesis about tissue-specificity imprinting and tissue residency of T cells.
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Improved survival of HIV-1-infected patients with progressive multifocal leukoencephalopathy receiving early 5-drug combination antiretroviral therapy.
PLoS ONE
PUBLISHED: 05-17-2011
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Progressive multifocal leukoencephalopathy (PML), a rare devastating demyelinating disease caused by the polyomavirus JC (JCV), occurs in severely immunocompromised patients, most of whom have advanced-stage HIV infection. Despite combination antiretroviral therapy (cART), 50% of patients die within 6 months of PML onset. We conducted a multicenter, open-label pilot trial evaluating the survival benefit of a five-drug cART designed to accelerate HIV replication decay and JCV-specific immune recovery.
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Interferon-alpha triggers B cell effector 1 (Be1) commitment.
PLoS ONE
PUBLISHED: 04-02-2011
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B-cells can contribute to the pathogenesis of autoimmune diseases not only through auto-antibody secretion but also via cytokine production. Therapeutic depletion of B-cells influences the functions and maintenance of various T-cell subsets. The mechanisms governing the functional heterogeneity of B-cell subsets as cytokine-producing cells are poorly understood. B-cells can differentiate into two functionally polarized effectors, one (B-effector-1-cells) producing a Th-1-like cytokine pattern and the other (Be2) producing a Th-2-like pattern. IL-12 and IFN-? play a key role in Be1 polarization, but the initial trigger of Be1 commitment is unclear. Type-I-interferons are produced early in the immune response and prime several processes involved in innate and adaptive responses. Here, we report that IFN-? triggers a signaling cascade in resting human naive B-cells, involving STAT4 and T-bet, two key IFN-? gene imprinting factors. IFN-? primed naive B-cells for IFN-? production and increased IFN-? gene responsiveness to IL-12. IFN-? continues this polarization by re-inducing T-bet and up-regulating IL-12R?2 expression. IFN-? and IFN-? therefore pave the way for the action of IL-12. These results point to a coordinated action of IFN-?, IFN-? and IL-12 in Be1 polarization of naive B-cells, and may provide new insights into the mechanisms by which type-I-interferons favor autoimmunity.
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Direct CD4 help provision following interaction of memory CD4 and CD8 T cells with distinct antigen-presenting dendritic cells.
J. Immunol.
PUBLISHED: 06-18-2010
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Accumulating evidence suggests that CD4 help is needed at the memory stage to mount effective secondary CD8 T cell responses. In this paper, we report that memory CD4 T cells can provide efficient help to memory CD8 T cells after interaction of the two lymphocytes with distinct dendritic cells. Provision of help to CD8 T cells required direct cell-cell contact and involved both IL-2 and CD40 ligation, within a CD4-CD8 T cell synapse. Thus, following antigenic interaction with APCs, activated memory CD4 and CD8 T cells appear to separate from their respective APCs before meeting each other for help provision, regardless of their Ag specificity. CD4 help for memory CD8 T cells therefore appears to be conditioned primarily not by Ag specificity but by activation status.
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CD25 appears non essential for human peripheral T(reg) maintenance in vivo.
PLoS ONE
PUBLISHED: 02-17-2010
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IL-2 has been reported to be critical for peripheral T(reg) survival in mouse models. Here, we examined T(reg) maintenance in a series of paediatric liver transplant recipients who received basiliximab, a therapeutic anti-CD25 monoclonal antibody.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

How does it work?

We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.