1,721,158 research outputs found
New frontiers in cell-based immunotherapy of cancer
No full textBackground: Cancer remains one of the leading causes of death. Over the past decade, discovery of tumor antigens, as well as new findings in basic immunology, have led to novel opportunities for developing active immunotherapeutical approaches for prevention and treatment of cancer. Objective/methods: This is a review of the literature and patents on the therapeutic potential of immune-based cell cancer therapies. Results/conclusion: In this article, we discuss the different approaches at present used for immune-based cell cancer therapies, and the results obtained both in preclinical models and in clinical trials of hematological malignancies and solid tumors
Targeting IL-23 in human diseases
No full textImportance of the field: IL-23 is one of the most intriguing cytokine for its many immunological functions, which are the basis of its important role in host defense but also of its possible contribution to the pathogenesis of several diseases.Areas covered in this review: The literature and patents about IL-23 pathway and their targeting in therapeutic potential applications. Findings published within the last 5 years receive particular attention.What the reader will gain: An overview of the emerging role of IL-23 in physiological and pathological conditions and a review of the different approaches (IL-23 pathway-based) currently used for autoimmune diseases and cancer therapies and the results obtained both in preclinical models and in clinical trials.Take home message: Inhibition/targeting of IL-23 may be a good and novel therapeutic strategy, especially in the treatment of diseases like psoriasis, for which current treatments show more pronounced side effects than those of IL-23-blocking and employed as part of specific patient-tailored therapies in inflammatory bowel diseases
The effect of Helicobacter pylori on asthma and allergy
Full text linkCurrent evidence indicates an inverse association between Helicobacter pylori and asthma and allergy. H. pylori is a Gram-negative bacterium which represents the major cause of peptic ulcer and gastric cancer, and preferentially elicits a T helper (Th)-1 response. Many H. pylori factors, such as the neutrophil-activating factor of H. pylori (HP-NAP), are able to drive Th-1 polarization and to display a powerful inhibition of allergic Th-2 response. This article proposes an overview of the actual knowledge about the effects of H. pylori on asthma and allergy. Special attention has been drawn to HP-NAP as a potential novel strategy for the prevention and treatment of asthma and atopy
The neutrophil-activating protein of Helicobacter pylori (HP-NAP) as an immune modulating agent
No full textDuring evolution microorganisms have developed several immune modulating strategies. The Helicobacter pylori neutrophil-activating protein (HP-NAP) is a virulence factor that attracts and activates neutrophils, and promotes their endothelial adhesion and the production of oxygen radicals and chemokines, including CXCL8, CCL3 and CCL4. HP-NAP, a TLR2 agonist, is an immune modulator able to induce the expression of interleukin-12 (IL-12) and IL-23 by human neutrophils and monocytes. In fact, HP-NAP has the potential to shift antigen-specific T-cell responses from a predominant Th2 to a polarized Th1 cytotoxic phenotype, characterized by high levels of interferon-gamma and tumor necrosis factor-alpha production. Thus, HP-NAP is a key factor driving Th1 inflammation in H. pylori infection and may be a new tool for future therapeutic strategies aimed at redirecting Th2 into Th1 responses, for example in atopy, vaccinology and cancer immunotherapy
, T cells and cytokines: the âdangerous liaisonsâ
No full textHelicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune gastritis. The type of host immune response against H. pylori is crucial for the outcome of the infection. A predominant H. pylori-specific Th1 response, characterized by high IFN-gamma, TNF-alpha, and IL-12 production associates with peptic ulcer, whereas combined secretion of both Th1 and Th2 cytokines are present in uncomplicated gastritis. Gastric T cells from MALT lymphoma exhibit abnormal help for autologous B-cell proliferation and reduced perforin- and Fas-Fas ligand-mediated killing of B cells. In H. pylori-infected patients with autoimmune gastritis cytolytic T cells infiltrating the gastric mucosa cross-recognize different epitopes of H. pylori proteins and H+K+ ATPase autoantigen. These data suggest that peptic ulcer can be regarded as a Th1-driven immunopathological response to some H. pylori antigens, whereas deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support the onset of low-grade B-cell lymphoma. Alternatively, If. pylori infection may lead in some individuals to gastric autoimmunity via molecular mimicry. (c) 2004 Federation of European Microbiological Societies. Published by Elsevier B.V. All rights reserved
Gastric autoimmunity: the role of Helicobacter pylori and molecular mimicry.
No full textPathogens can induce autoreactive T cells to initiate autoimmune disease by several mechanisms. Pathogen-induced inflammation results in the enhanced presentation of self antigens, which causes the expansion of the activated autoreactive T cells that are required for disease onset. Alternatively, a pathogen might express antigens with epitopes that are structurally similar to epitopes of autoantigens, resulting in a mechanism of molecular mimicry. This is the case for Helicobacter pylori-associated human autoimmune gastritis, in which the activated CD4+ Th1 cells that infiltrate the gastric mucosa cross-recognize the epitopes of self gastric parietal cell H(+)K(+)-ATPase and of various H. pylori proteins. Therefore, in genetically susceptible individuals, H. pylori infection can start or worsen gastric autoimmunity, leading to atrophic gastritis
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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