Lymphoreticular system

Peripheral pathogenesis involves the lymphoreticular system 794 Prion disease produces characteristic pathology in the central nervous system 795... 

Peripheral pathogenesis involves the lymphoreticular system. Although the pathological consequences of prion infection occur in the central nervous system, and experimental transmission of these diseases is most efficiently accomplished by intracerebral inoculation, most natural infections do not occur by these means. Indeed, administration to sites other than the central nervous system is known to be associated with much longer incubation periods, which may extend to 20 years or more [5,12]. Experimental evidence suggests that this latent period is associated with clinically silent prion replication in... 

Abbreviations used to Identify Tumor Lines of Mouse Lymphoreticular System... 

Although several animal studies have found histological alterations in the lymphoreticular system, in particular granulomas in the hilar lymph nodes, these effects are secondary to the pulmonary effects (Steinhagen et al. 1978 Thomson et al. 1986) and resulted from the removal of aluminum from the lungs by alveolar macrophages. 

Immunotoxicity. There are currently no in vivo studies in humans or animals that examined immunocompetence following exposure to DEHP by any route of exposure. No histopathological alterations to organs of the lymphoreticular system due to treatment with DEHP were reported by any animal study. DEHP does bind to mononuclear leukocytes in vitro (Sager and Little 1989) but this is not an inherently toxic phenomenon. The overall evidence suggests that the immune system is not a target for DEHP toxicity. Specific studies addressing this issue do not seem necessary at this time. 

No information was located regarding the effects of uranium on the immunological and lymphoreticular system in humans and animals following dermal exposure for any duration. 

Immunotoxicity. No studies were located regarding the immunotoxicity of 1.1.1-trichloroethane in humans. Information regarding the lymphoreticular system was limited to reports of spleen congestion in subjects acutely exposed to high levels of 1.1.1-trichloroethane (Gresham and Treip 1983 Stahl et al. 1969). Exposed mice were not more susceptible to bacterial infection than unexposed control mice after a single inhalation exposure to 1.1.1-trichloroethane (Aranyi et al. 

Very limited information exists regarding histology and function of tissues of the lymphoreticular system after 1.1.1-trichloroethane exposure by any route. Histological evaluation of lymphoreticular tissues, including lymph nodes, thymus, and spleen, revealed no lesions attributable to 1.1.1 -trichloroethane exposure (Adams et al. 1950 Calhoun et al. 1981 Kjellstrand et al. 1985b Prendergast et al. 1967 Torkelson et al. 1958). 

In animals, profound effects on the immune and lymphoreticular systems were sequelae of exposure to radioactive strontium by the inhalation or oral routes. Lymphopenia and immunosuppression (reduced antibody titers) were noted in beagles exposed to soluble aerosols of 90SrCl2. In beagles exposed by... 

Fig. 3. Model of the life cycle of prions. PrP is synthesized in the rough endoplas-matic reticulum (ER), and after passing through the secretory pathway including the Golgi and secretory vesicles, reaches the surface of a PrP infectable cell where it is anchored via a glycosylphosphatidyl inositol (GPI) moiety. Endocytosis of PrP and possibly PrP via clathrin coated vesicles could be mediated by the 37 kDa laminin receptor precursor (LRP). The uptake of the infectious agent could also be LRP independent. The conversion of the internalized PrP to PrP is thought to take place in the endo-somes, lysosomes, or endolysosomes. Molecular chaperones could be involved in this conversion process. PrP replication and aggregation can occur in neuronal cells of the brain but also in the cells constituting the lymphoreticular system. Alternatively, endocytosis and conversion of PrP into PrP could happen in caveolae-like domains (CLDs).

One knows that this protein is encoded by a single exon, in humans called the PRNP gene. It is primarily found on the cell surface of neurons, glial cells, and cells of the lymphoreticular system, and it is anchored in these cell membranes via a glcosyl-phosphatidyl-inositol group. The protein is also detected at low concentrations in muscle cells and cells of the immune system. 

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