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At least 361 records · Page 20Linked to original sources
PubMed2002

Dendritic cell subtypes in autoimmune liver diseases; decreased expression of HLA DR and CD123 on type 2 dendritic cells.

In order to dissect the role of different subsets of antigen-presenting dendritic cell (DC) in autoimmune liver diseases, we analyzed the frequencies and phenotypes of DC1 and DC2 from patients with primary biliary cirrhosis (PBC) and autoimmune hepatitis (AIH). The numbers of DC, DC1 and DC2 in a fixed amount of peripheral blood (20 ml) from 14 patients with PBC (therapy [-]: 5, therapy [+]: 9), seven patients with AIH (therapy [-]): 4, therapy [+]: 3), nine patients with chronic hepatitis due to hepatitis C virus and 12 healthy subjects were estimated using three-color flow cytometry. The mean fluorescence intensities of HLA DR, CD11c and CD123 on DC subsets were evaluated from the flow cytometric profiles. The numbers of DC1 and DC2 did not differ significantly among patients and controls. The expression of HLA DR was lower on DC1 from patients with AIH, but not on PBC. However, the levels of HLA DR and CD 123 on DC2 were significantly decreased in patients with PBC (therapy [-]) and AIH (therapy [-]) compared with healthy subjects (P<0.05). Defective phenotype of DC2 in both AIH and PBC may have a relevance to the breakdown of tolerance to self antigen in these autoimmune diseases. Functional study of DC2 in autoimmune liver diseases is warranted.

Journal Article↗
PubMed1982

Dendritic reticulum cell sarcoma? Four cases of a lymphoma probably derived from dendritic reticulum cells of the follicular compartment.

This paper describes the histological picture of four tumours of the follicular compartment of the lymph node, in which the proliferating cell appeared to be the dendritic reticulum cell (DRC). This assumption was based on the results of light microscopical, ultrastructural, immunological, and enzymehistochemical investigations. The tumour cells resembled DRC's closely in (1) the striking pattern of interdigitations and occasional tight junction-like contacts between the neoplastic cells on electron microscopical analysis; (2) presence of receptors for the activated third component of complement on the membrane of the cells; (3) absence of monoclonal immunoglobulins and T-cell antigen on the surface and of lysozyme, alpha 1-antitrypsin or alpha 1-antichymotrypsin in the cytoplasm of the neoplastic cells. Moreover, (4) the tumour cells showed moderate alpha-naphtyl acetate esterase, weak to absent acid phosphatase and (with one exception) strong 5-nucleotidase activity. Furthermore, (5) the neoplastic cells expressed Ia-like antigens on the surface in all four cases. The relation with follicle centre cell lymphomas, the differential diagnosis and clinical data are discussed.

Adult↗
PubMed2003

The interaction between NK cells and dendritic cells in bacterial infections results in rapid induction of NK cell activation and in the lysis of uninfected dendritic cells.

NK and DC reciprocal interactions have only recently been investigated. In this study, we focused on the interplay between NK cells and DC in two models of bacterial infection. Immature monocyte-derived DC were cultured in the presence of live Escherichia coli or bacillus Calmette-Guérin. Upon exposure to either extracellular or intracellular bacteria, DC underwent maturation as assessed by the increased levels of expression of CD80,CD86, and HLA molecules and the de novo expression of CD83 and CCR7. Significant amounts of TNF-alpha and IL-12 were released by DC upon infection, whereas IL-2 and IL-15 were barely detectable in culture supernatants. Both infected and uninfected DC were capable of inducing in fresh autologous NK cells the expression of CD69 and HLA-DR and of inducing cell proliferation. Remarkably, however, infected DC were much stronger inducers of NK cell activation and proliferation than uninfected DC. Thus, after just 24 h of NK/DC coculture, only those NK cells that had been exposed to bacteria-infected DC had acquired the ability to lyse autologous immature DC. In addition, infected DC were more resistant to NK-mediated lysis as a consequence of the up-regulation of HLA class I molecule expression on their surface. This study suggests a regulatory circuit involving NK cells and DC in which DC-induced NK cell activation is effectively enhanced by the presence of pathogens. Activated NK cells, by limiting the supply of immature DC, may then exert a control on subsequent innate and adaptive immune responses.

Antigens, CD↗
PubMed2003

Outer membrane protein A renders dendritic cells and macrophages responsive to CCL21 and triggers dendritic cell migration to secondary lymphoid organs.

Outer membrane protein A (OmpA) is a class of bacterial cell wall protein that is immunogenic without adjuvant. As specific immune responses are initiated in the lymph nodes (LN, we analyzed the effect of the OmpA from Klebsiella pneumoniae (KpOmpA) onchemokine/ chemokine receptor expression by APC and on cell migration to the LN. Upon contact with KpOmpA, human immature DC and macrophages acquire CCR7 expression and responsiveness to CCL21. In parallel, CCR1 and CCR5 expression is down-regulated and CXCL8, CCL2, CCL3 and CCL5 production is up-regulated. Mice injected subcutaneously with KpOmpA present a transient inflammatory reaction at the site of injection accompanied by an enlargement of the draining LN with a higher proportion of DC and macrophages. Lastly, when exposed to KpOmpA prior injection, DC but not macrophages migrate to the draining LN. In conclusion, KpOmpA confers a migratory phenotype to DC and triggers their migration to the regional LN. This property contributes to explain how innate cells initiate adaptive immune response upon recognition of conserved bacterial components and also why OmpA is immunogenic in the absence of adjuvant.

Adoptive Transfer↗