191 research outputs found
Evaluation of the ability of Helicobacter pylori in inducing the production of B cells activating factors: possible implications in the development of MALT lymphomas
No full textUpdates in histiocytic and dendritic cell proliferations and neoplasms
No full textTumours derived from histiocytes/macrophages and from dendritic cells are extremely rare. They mainly occur in lymphoid tissues, where they account for less than 1% of tumours, but they can be also found in extranodal sites. These neoplasms represent a heterogeneous group of diseases with a variable clinical behavior even within the same tumour entity, ranging from localized and indolent forms to systemic aggressive processes. Diagnosis is based on histological and immunophenotypic features, but overlaps occur across diseases with different biological nature and clinical course, thus correlation with clinical and radiological features is sometimes necessary for final diagnosis. The driver mutations identified during the last few years contributed to a better understanding of the pathogenesis of some of these tumours and in some of them turned out to be useful for diagnosis and treatment
Neoplasms derived from plasmacytoid monocytes/interferon-producing cells: variability of CD56 and granzyme B expression.
No full textAuthor's reply 1492-1483
Evaluation of the ability of Helicobacter pylori in inducing the production of B cells activating factors: possible implications in the development of MALT lymphomas
No full textA human natural killer cell subset provides an innate source of IL-22 for mucosal immunity.
No full textNatural killer (NK) cells are classically viewed as lymphocytes that provide innate surveillance against virally infected cells and tumour cells through the release of cytolytic mediators and interferon (IFN)-gamma. In humans, blood CD56(dim) NK cells specialize in the lysis of cell targets. In the lymph nodes, CD56(bright) NK cells secrete IFN-gamma cooperating with dendritic cells and T cells in the generation of adaptive responses. Here we report the characterization of a human NK cell subset located in mucosa-associated lymphoid tissues, such as tonsils and Peyer's patches, which is hard-wired to secrete interleukin (IL)-22, IL-26 and leukaemia inhibitory factor. These NK cells, which we refer to as NK-22 cells, are triggered by acute exposure to IL-23. In vitro, NK-22-secreted cytokines stimulate epithelial cells to secrete IL-10, proliferate and express a variety of mitogenic and anti-apoptotic molecules. NK-22 cells are also found in mouse mucosa-associated lymphoid tissues and appear in the small intestine lamina propria during bacterial infection, suggesting that NK-22 cells provide an innate source of IL-22 that may help constrain inflammation and protect mucosal sites
Characterization of the cross-talk between human neutrophils and a subset of pro-inflammatory dendritic cells
No full textNeutrophils represent key components of the innate immune system with the ability not only to phagocytose and killing invading pathogens, but also to produce a variety of proteins, including cytokines and chemokines, with important consequences on the recruitment and activation of other immune cells, such as monocytes, dendritic cells, T and B cells. For instance, it has been shown that neutrophils can directly interact with, and induce functional maturation of, immature monocyte-derived dendritic cells (moDC). Indeed, upon interaction with neutrophils, moDC up-regulate the expression of costimulatory molecules, such as CD83, CD86 and CD40, and secrete IL-12, thus acquiring the ability to induce proliferation and Th1 polarization of naïve T cells. In order to extend these findings, the present study was designed to address whether human neutrophils interact with peripheral blood-derived dendritic cells and the pathological consequences that such interaction could eventually produce. In human peripheral blood, dendritic cells can be divided in plasmacytoid dendritic cells (pDC) and myeloid dendritic cells (mDC), the latter further divided in three different subsets based on the expression of CD1c, BDCA-3, and CD16. By analyzing different chronic inflammatory pathologies, such as Crohn's disease, psoriasis and Sweet's syndrome, we found that neutrophils co-localize with a subtype of myeloid dendritic cells (mDC) with characteristics resembling the CD16+ subset of mDC. In order to characterize the interaction between the two cell types, autologous neutrophils, highly purified by an in-house built immunonegative selection protocol, and CD16+ DC were isolated from healthy donors and analyzed in a co-culture system under different stimulatory conditions. Here we show that neutrophils modulate different effector functions of CD16+ DC, including their survival and their ability to produce IL-12p70. Besides providing the basis for a better understanding of the cellular interactions that occur in pathological conditions, our results further emphasize the importance of neutrophils in the modulation of the inflammatory response
slanDCs in carcinoma-draining lymph nodes.
No full textDendritic cells (DCs) are known to initiate adaptive immune responses against malignant cells. However, the role in anticancer immunosurveillance of 6-sulfo LacNAc-expressing DCs (slanDCs), a distinct population of circulating and tissue-resident pro-inflammatory DCs, is unclear. We have recently demonstrated the involvement of slanDCs in nodal immune responses against carcinoma cells
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