The activity of purine salvage pathway enzymes in murine and horse models of congenital and acquired dysimmunity

James J. Castles, M. Eric Gershwin, Wilfred Saito, Alex Ardans, Bennie Osburn

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Abstract

Previous studies of human congenital immunodeficiency states and in vitro observations of lymphocyte response to mitogens have implicated two purine salvage pathway enzymes, adenosine deaminase (ADA) and nucleoside phosphorylase (NP), as critical in the normal maturation and/or function of the immune system. Based on this information, ADA and NP activities were examined in a variety of congenital and acquired animal models of dysimmunity. The animals studied herein included: congenitally athymic (nude) mice; congenitally asplenic mice; congenitally athymic-asplenic mice; motheaten mice; New Zealand mice; and Arabian foals with severe combined immunodeficiency. No significant differences in the activities of ADA and NP were observed in any of these animals when compared with either normal littermates or animals with intact immune function. Major species differences were apparent when erythrocyte ADA activity was compared between mice and horses. In contrast, only minor strain alterations in ADA or NP activity were noted between several inbred groups of mice.

Original languageEnglish (US)
Pages (from-to)165-173
Number of pages9
JournalDevelopmental and Comparative Immunology
Volume1
Issue number2
DOIs
StatePublished - 1977

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Adenosine Deaminase
Horses
Nude Mice
Enzymes
Severe Combined Immunodeficiency
New Zealand
Mitogens
Immune System
Animal Models
Erythrocytes
purine
Lymphocytes
nucleoside phosphorylase
adenosine phosphorylase

ASJC Scopus subject areas

  • Developmental Biology
  • Immunology

Cite this

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abstract = "Previous studies of human congenital immunodeficiency states and in vitro observations of lymphocyte response to mitogens have implicated two purine salvage pathway enzymes, adenosine deaminase (ADA) and nucleoside phosphorylase (NP), as critical in the normal maturation and/or function of the immune system. Based on this information, ADA and NP activities were examined in a variety of congenital and acquired animal models of dysimmunity. The animals studied herein included: congenitally athymic (nude) mice; congenitally asplenic mice; congenitally athymic-asplenic mice; motheaten mice; New Zealand mice; and Arabian foals with severe combined immunodeficiency. No significant differences in the activities of ADA and NP were observed in any of these animals when compared with either normal littermates or animals with intact immune function. Major species differences were apparent when erythrocyte ADA activity was compared between mice and horses. In contrast, only minor strain alterations in ADA or NP activity were noted between several inbred groups of mice.",
author = "Castles, {James J.} and Gershwin, {M. Eric} and Wilfred Saito and Alex Ardans and Bennie Osburn",
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T1 - The activity of purine salvage pathway enzymes in murine and horse models of congenital and acquired dysimmunity

AU - Castles, James J.

AU - Gershwin, M. Eric

AU - Saito, Wilfred

AU - Ardans, Alex

AU - Osburn, Bennie

PY - 1977

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N2 - Previous studies of human congenital immunodeficiency states and in vitro observations of lymphocyte response to mitogens have implicated two purine salvage pathway enzymes, adenosine deaminase (ADA) and nucleoside phosphorylase (NP), as critical in the normal maturation and/or function of the immune system. Based on this information, ADA and NP activities were examined in a variety of congenital and acquired animal models of dysimmunity. The animals studied herein included: congenitally athymic (nude) mice; congenitally asplenic mice; congenitally athymic-asplenic mice; motheaten mice; New Zealand mice; and Arabian foals with severe combined immunodeficiency. No significant differences in the activities of ADA and NP were observed in any of these animals when compared with either normal littermates or animals with intact immune function. Major species differences were apparent when erythrocyte ADA activity was compared between mice and horses. In contrast, only minor strain alterations in ADA or NP activity were noted between several inbred groups of mice.

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