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Molecular pathology of severe combined immunodeficiency in mice, horses, and dogs Perryman LEVet Pathol 2004[Mar]; 41 (2): 95-100Severe combined immunodeficiency (SCID) is an inherited disorder of humans, mice, horses, and dogs, in which affected individuals are incapable of generating antigen-specific immune responses. It occurs when lymphocyte precursors fail to differentiate into mature lymphocytes because of mutations within recombinase-activating genes 1 and 2 or within the genes encoding deoxyribonucleic acid (DNA)-dependent protein kinase (DNA-PK). It also occurs when differentiated lymphocytes are incapable of completing signal transduction pathways because of defects in cell surface receptors for interleukins (IL). A spontaneous mutation in DNA-PKcs of BALB/c mice results in SCID, as do experimentally induced mutations in RAG1 and RAG2. SCID in horses results from a spontaneous mutation in DNA-PKcs. Two molecular mechanisms account for SCID in dogs. Jack Russell Terriers have a mutation within the DNA-PKcs gene, whereas Cardigan Welsh Corgi and Basset Hound have different defects in the gene encoding the gamma chain that is common to the receptors for IL-2, -4, -7, -9, -15, and -21. The location of the mutation within target genes influences the spectrum of diseases observed in affected animals.|*DNA-Binding Proteins[MESH]|Animals[MESH]|DNA-Activated Protein Kinase[MESH]|Dog Diseases/*genetics[MESH]|Dogs[MESH]|Genes, RAG-1/genetics[MESH]|Genes, Recessive/genetics[MESH]|Horse Diseases/*genetics[MESH]|Horses[MESH]|Immunoglobulin gamma-Chains/genetics[MESH]|Lymphocytes/*pathology[MESH]|Mice[MESH]|Mutation/genetics[MESH]|Protein Serine-Threonine Kinases/genetics[MESH]|Rodent Diseases/*genetics[MESH]|Severe Combined Immunodeficiency/genetics/*veterinary[MESH]|Signal Transduction/genetics[MESH] |
