Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In op/op mice, immunohistochemical and electron microscopic techniques were used to examine the effects of the OP mutation on dendritic cell populations in lymphoid tissues and skin. In the thymic medulla, T cell zone of lymph nodes, and splenic white pulp of op/op mice, numbers of NLDC-145-positive dendritic cells were not decreased. Compared to the normal littermates, numbers of BM8-positive macrophages were reduced in various tissues of the mutant mice, including the lymphoid tissues. These dendritic cells of op/op mice expressed Ia antigens but not F4/80 and BM8 antigens. Ultrastructurally, the dendritic cells developed a tubulovesicular system typical of interdigitating cells, but they were abnormal in that interdigitation of their cytoplasmic processes was not prominent. In the epidermis of the op/op mice, dendritic cells expressed NLDC-145, F4/80, Ia antigens, and adenosine diphosphatase or adenosine triphosphatase activity, and numbers of NLDC-145-, Ia-, or ADPase-positive dendritic cells were reduced slightly, but these reductions were not significant statistically. Birbeck granules were detected in most of them electron microscopically. These results indicate that nonlymphoid dendritic cells develop in the lymphoid tissues and skin of op/op mouse, suggesting that they are differentiated from granulocyte-macrophage colony-forming cells or earlier hematopoietic cell precursors.
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PMID:Differentiation of dendritic cell populations in macrophage colony-stimulating factor-deficient mice homozygous for the osteopetrosis (op) mutation. 842 88

The immunohistochemical study of chamois (Rupicapra rupicapra L.) skin showed that a limited number of available monoclonal and polyclonal antibodies expressed reactivity with skin cell components. These included cytokeratins, vimentin, desmin, neuron-specific enolase and S-100 protein with almost the same distribution pattern as already described in the skin of humans and animals. Antibodies used for labelling skin-associated lymphoid tissues and other cells with the immunologic function in human skin failed to demonstrate these cells in the chamois skin with the exception of LCA and OKT6 antibodies. Epidermal Langerhans cells were reliably demonstrated only by the enzyme histochemical method for adenosine triphosphatase, while the majority of mononuclear cells in dermal infiltrates showed a strong immunoreaction with OKT6 antibody. The histologic and histochemical analysis showed that the dermal infiltrations in infested skin consisted of macrophages, lymphocytes, granulocytes, mastocytes and fibroblasts. The chamois skin affected with sarcoptes mange showed a significant loss of cytokeratins in the epidermis and its derivatives. Particular keratinocytes showing nonspecific staining with several antibodies were also described and discussed in this paper.
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PMID:Immunohistochemical study of normal and mange (S. scabiei var. rupicaprae) infested chamois (Rupicapra rupicapra L.) skin. 965 47

Extracellular ATP and adenosine are important regulators of immune responses; however, contribution of purinergic signaling to host defense during persistent microbial infections remains obscure. Lyme borreliosis is a common arthropod-borne infection caused by Borrelia burgdorferi sensu lato. In this study, we investigated whether lymphoid purinergic signaling contributes to the mechanisms by which borreliae species evade the immune system and trigger joint inflammation. Intracutaneous inoculation of Borrelia garinii to C3H/He mice induced symptomatic infection manifested in elevated levels of borrelia-specific IgG Abs, persistent spirochete dissemination into the tissues and joint swelling, as well as approximately 2- to 2.5-fold enlargement of draining lymph nodes with hyperplasia of B cell follicle area and L-selectin shedding from activated T lymphocytes. Purine catabolism was also activated in lymph nodes but not spleen and blood of infected C3H/He mice within the first 4 postinfection weeks, particularly manifested in transient upregulations of adenosine triphosphatase/ectonucleoside triphosphate diphosphohydrolase and ecto-5'-nucleotidase/CD73 on CD4(+)CD8(+) T lymphocytes and adenosine deaminase activity on B220(+) B lymphocytes. Compared with borrelia-susceptible C3H/He strain, lymphocytes from C57BL/6 mice displayed markedly enhanced adenosine-generating capability due to approximately three times higher ratio of ecto-5'-nucleotidase to adenosine deaminase. Borrelia-infected C57BL/6 mice efficiently eradicated the inoculated spirochetes at more chronic stage without any signs of arthritis. Strikingly, deletion of key adenosine-generating enzyme, ecto-5'-nucleotidase/CD73, was accompanied by significantly enhanced joint swelling in borrelia-infected CD73-deficient C57BL/6 mice. Collectively, these data suggest that insufficient basal adenosine level and/or pathogen-induced disordered lymphoid purine homeostasis may serve as important prerequisite for promotion of inflammatory responses and further host's commitment to persistence of bacterial infection and arthritis development.
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PMID:Disordered lymphoid purine metabolism contributes to the pathogenesis of persistent Borrelia garinii infection in mice. 2035 56


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