Abstract
It is controversially discussed whether immune-deficient mice experience severity in the absence of infection. Because a comprehensive analysis of the well-being of immune-deficient mice under specific pathogen free conditions is missing, we used a multi-parametric test analyzing, corticosterone, weight, nest building and facial expression over a period of 9 month to determine the well-being of two immune-deficient mouse lines (recombination activating gene 2- and interferon gamma receptor-deficient mice). We do not find evidence for severity when comparing immune-deficient mice to their heterozygous immune-competent littermates. Our data challenge the assumption that immune-deficiency per se regardless of housing conditions causes severity. Based on our study we propose to use objective non-invasive parameters determined by laboratory animal science for decisions concerning severity of immune-deficient mice.
Highlights
Mice with genetic alterations in immunologically relevant genes are frequently used in research
Analysis of long-term corticosterone levels measured in fur samples of the same mice after weaning, in young adults and at nine months of age revealed neither statistically significant nor biologically relevant differences when comparing immune-deficient mice to their immune-competent littermate controls
In lung Pneumocyte Typ II-Hyperplasia (PT2H) had a similar distribution between the groups, Bronchus Associated Lymphoid tissue (BALT)—hyperplasia was more often observed in mice with IFNγR+/- than with IFNγR-/- genotype and acidophilic
Summary
Mice with genetic alterations in immunologically relevant genes are frequently used in research. Other studies reported differences between immune-deficient and -competent mice based on physiological or behavioral alterations [3,4,5,6,7]. In the current study we investigated well-being of two immune-deficient mouse lines, one being deficient in recombination activating gene 2 (Rag-/-) resulting in lack of functional T cells and B cells and the other lacking expression of the interferon gamma receptor 1 gene (IFNγR-/-). Both genetic defects cause severe immune-deficiency in humans. Mice were sacrificed and a pathological analysis of inner organs was performed
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