In SCID mice recessive mutation in 16 chromosome responsible for deficient activity of Prcdc enzime involved into DNA repair takes place. This really results in deficiency in V(D)J recombination, but not absolute absence of T and B cells. Therefore, experimental models using SCID mice are at some extent "leaky". So, study performed on SCID mice may result in hardly interpretable results. It would be better to use RAG knockout mice.

For transplantation studies or tumor xenografts SCID mice are acceptable unless you need NK cells for ADC activity.

As indicated in the previous response SCID mice are a congenic mouse that possesses both genetic autosomal recessive mutations SCID (Prkdcscid;DNA-dependent protein kinase, catalytic subunit, chrom 16--https://www.wikigenes.org/e/gene/e/5591.html ) and beige (Lystbg; lysosomal trafficking regulator; chrom 13--https://www.wikigenes.org/e/gene/e/17101.html). The SCID mutation results in severe combined immunodeficiency affecting both the B and T lymphocytes. The beige mutation results in defective natural killer (NK) cells.

Overall Immune Properties:

• Severe lymphopenia (lack both T-cells and B-cells)
• Diminished Natural Killer (NK) cell activity relative to other SCID models
• Rudimentary thymus
• Highly susceptible to opportunistic viral and bacterial infection.
• This mouse was developed by Croy, et al. at the University of Guelph by an intercross of C.B-17 SCID/SCID to C57BL/6 bg/bg mice and licensed to Charles River in 1993.

A few references available on PubMed include:

http://www.ncbi.nlm.nih.gov/pubmed/9143737 http://www.ncbi.nlm.nih.gov/pubmed/12384415

Websites for supplies such as Harlon, Charles River, Jackson Labs and Taconic provide addition information on these and related immunodeficient mouse strains.

Does the defective NK cell activity also affect NK regard of cell number and development?

Thank you for answering in advance.

Chung Hsiang