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Pristane retards clearance of particulate materials from the peritoneal cavity of laboratory mice.

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The effect of intraperitoneal pristane on the movement of India ink particles and water-based radio-opaque dye injected into the peritoneal cavity of mice was examined. There was a marked difference between pristane-treated mice and unmanipulated controls in terms of particle retention;

Regulation of Leukocyte Recruitment to the Spleen and Peritoneal Cavity during Pristane-Induced Inflammation.

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Chronic inflammation is associated with an increased number of leukocytes in the spleen, which are then redirected to the site of inflammation. However, it remains unknown how leukocyte recruitment is regulated. Herein, chronic inflammation was induced by intraperitoneal injection of pristane into

Pristane-induced arthritis is CD4+ T-cell dependent.

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The development of arthritis induced in mice by intraperitoneal injection of the non-antigenic mineral oil pristane (2,6,10,14-tetramethylpentadecane) was shown to depend on the presence of CD4+ T cells. Initial experiments assessed the influx of lymphoid cells into the peritoneal cavity of CBA/Igb

Distinct granuloma responses in C57BL/6J and BALB/cByJ mice in response to pristane.

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Granuloma formation is an inflammatory response of the host against invading pathogens or indigestible substances. We generated mesenteric oil granulomas by injecting pristane into the peritoneal cavity (PC) of mice, and compared oil granuloma formation in the C57BL/6J and BALB/cByJ strains of mice.

The accelerating role of Abelson murine leukemia virus in murine plasmacytoma development: in vitro infection of spleen cells generates donor-type tumors after transfer to pristane-treated BALB/c mice.

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The role of Abelson murine leukemia virus (A-MuLV) in the accelerated development of murine plasmacytomas (PCs) (Potter et al., 1973: Science, 132, 592-594) was studied in a new experimental system. Spleen cells from pristane-treated or untreated BALB/c mice carrying Robertsonian 6;15 fusion

Increased NHC Cells in the Peritoneal Cavity of Plasmacytoma Susceptible BALB/c Mouse.

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BALB/c strain mice are unique in that they develop murine plasmacytoma (MPC) as a consequence of the inflammation induced by pristane oil injection in the peritoneal cavity. In this work the Treg, Th17, B1, B2, and NHC lymphocyte populations from the peritoneal environment of BALB/c, the susceptible

Differential development of oil granulomas induced by pristane injection in galectin-3 deficient mice.

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BACKGROUND Galectin-3 is known to be a lectin that plays an important role in inflammatory processes, acting as pro-inflammatory mediator in activation and migration of neutrophils and macrophages, as well as in the phagocytic function of these cells. The injection of mineral oils into the

X-linked immunodeficient mice spontaneously produce lupus-related anti-RNA helicase A autoantibodies, but are resistant to pristane-induced lupus.

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Murine lupus can occur spontaneously or be induced by hydrocarbons, such as pristane. Spontaneous disease in MRL and NZB/W F1 mice is suppressed by the xid (X-linked immunodeficiency) mutation, which greatly diminishes T cell-independent type 2 responses as well as the number of peritoneal B1 cells.

In vitro mutagenicity of the plasmacytomagenic agent pristane (2,6,10,14-tetramethylpentadecane).

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Pristane is known to induce a distinct type of B-cell-derived malignant lymphoma, plasmacytoma, after administration into the peritoneal cavity of genetically susceptible BALB/cAnPt mice. Since the mechanism of pristane-induced plasmacytoma development is poorly understood, we chose to examine the

Suppression of Autoimmunity and Renal Disease in Pristane-Induced Lupus by Myeloperoxidase.

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OBJECTIVE Myeloperoxidase (MPO) locally contributes to organ damage in various chronic inflammatory conditions by generating reactive intermediates. The contribution of MPO in the development of experimental lupus is unknown. The aim of this study was to define the role of MPO in murine lupus

Damage to surface membrane of Schistosoma mansoni by pristane (2, 6, 10, 14 tetramethyl pentadecane) and other hydrophobic compounds.

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Intraperitoneal injection of cercariae into pristane (2, 6, 10, 14 tetramethyl pentadecane)-primed Balb/c mice led to greatly diminished numbers of portal and peritoneal worms compared with untreated mice. Schistosomula taken from the peritoneal cavity of pristane-primed mice carried globules of

Induction of apoptosis by the hydrocarbon oil pristane: implications for pristane-induced lupus.

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Intraperitoneal injection of the hydrocarbon oil pristane into normal mice leads to a lupus-like autoimmune syndrome. Although advances in defining the roles of cellular and humoral mediators involved in this syndrome have been made, the mechanisms that initiate a break in tolerance leading to

Pristane-induced granulocyte recruitment promotes phenotypic conversion of macrophages and protects against diffuse pulmonary hemorrhage in Mac-1 deficiency.

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Diffuse pulmonary hemorrhage (DPH) is an uncommon but critical complication of systemic lupus erythematosus. Peritoneal administration of 2,6,10,14-tetramethylpentadecane (pristane) can recapitulate a lupus-like syndrome in mice, which can develop into DPH within a few weeks, especially in C57BL/6

Fas and Fas ligand mutations inhibit autoantibody production in pristane-induced lupus.

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Mutations of Fas (lpr) or Fas ligand (gld) cause a limited lupus-like syndrome in B6 mice by interfering with the deletion of autoreactive B and/or T cells. A more generalized lupus syndrome reminiscent of that of MRL mice can be induced in nonautoimmune strains by pristane, which causes a

Galectin-3 orchestrates the histology of mesentery and protects liver during lupus-like syndrome induced by pristane.

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Galectin-3 (Gal-3) controls intercellular and cell-extracellular matrix interactions during immunological responses. In chronic inflammation, Gal-3 is associated with fibrotic events, regulates B cell differentiation and delays lupus progression. Gal-3 deficient mice (Lgals3^-/-) have

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