A new mutation, <i>aly</i>, that induces a generalized lack of lymph nodes accompanied by immunodeficiency in mice

TLDR

The aly mutant mouse may serve as a model for primary immunodeficiency, similar to nu and scid mice. The authors propose the name alymphoplasia (gene symbol uly) for this mutant. The aly mutation leads to a complete absence of lymph nodes and Peyer’s patches, loss of defined lymphoid follicles in the spleen, lack of cortical‑medullary distinction in the thymus, severe humoral and cell‑mediated immunodeficiency with markedly reduced IgM, IgG, and IgA, failure to reject allogeneic skin grafts, yet mature T and B cells, and bone‑marrow transplant studies implicate a mesenchymal defect as the underlying cause.

Abstract

Abstract We have found a new spontaneous autosomal recessive mutation in mice that causes a systemic absence of lymph nodes and Peyer's patches. The name “alymphoplasia”, with the gene symbol “uly” , is proposed for this mutant. The spleen of alylay mice is devoid of well‐defined lymphoid follicles, and the thymus does not show a clear cortical‐medullary distinction. The mutant homozygotes are deficient in both humoral and cell‐mediated immune functions, and are highly susceptible to infections. They have a reduced level of IgM and severely depressed levels of IgG and IgA in their sera, and do not reject allogeneic skin grafts. However, they have mature T and B cells as determined from their cell surface antigens. The results of bone marrow transplantation experiments suggest a mesenchymal disorder as a possible cause of the lack of lymph nodes and of immunodeficiency in the aly mouse. The aly mutant mouse may be a useful animal model of primary immunodeficiency, as are the nu (nude) and scid (severe combined immunodeficiency) mice.