The SCID mouse mutant: definition, characterization, and potential uses - PubMed (original) (raw)
Review
The SCID mouse mutant: definition, characterization, and potential uses
M J Bosma et al. Annu Rev Immunol. 1991.
Abstract
Mice homozygous for the scid mutation (scid mice) are severely deficient in functional B and T lymphocytes. The mutation appears to impair the recombination of antigen receptor genes and thereby causes an arrest in the early development of B and T lineage-committed cells; other hematopoietic cell types appear to develop and function normally. The arrest in lymphocyte development is not absolute; some young adult scid mice are "leaky" and generate a few clones of functional B and T cells. By 10-14 months of age, virtually all scid mice are leaky. Scid mice readily support normal lymphocyte differentiation and can be reconstituted with normal lymphocytes from other mice and even partially reconstituted with human lymphocytes. They also support the growth of allogeneic and xenogeneic tumors. Thus, scid mice are of interest for studies of both normal and abnormal lymphocyte development and function. In addition, they can be used to study the function of nonlymphoid cell types in the absence of lymphocytes.
Similar articles
- The SCID mouse.
Pla M, Mahouy G. Pla M, et al. Nouv Rev Fr Hematol (1978). 1991;33(6):489-91. Nouv Rev Fr Hematol (1978). 1991. PMID: 1818304 Review. - T-cell receptor gene rearrangements in functional T-cell clones from severe combined immune deficient (scid) mice: reversion of the scid phenotype in individual lymphocyte progenitors.
Petrini JH, Carroll AM, Bosma MJ. Petrini JH, et al. Proc Natl Acad Sci U S A. 1990 May;87(9):3450-3. doi: 10.1073/pnas.87.9.3450. Proc Natl Acad Sci U S A. 1990. PMID: 2159151 Free PMC article. - T cell receptor-negative thymocytes from SCID mice can be induced to enter the CD4/CD8 differentiation pathway.
Shores EW, Sharrow SO, Uppenkamp I, Singer A. Shores EW, et al. Eur J Immunol. 1990 Jan;20(1):69-77. doi: 10.1002/eji.1830200111. Eur J Immunol. 1990. PMID: 1968394 - B and T cell leakiness in the scid mouse mutant.
Bosma MJ. Bosma MJ. Immunodefic Rev. 1992;3(4):261-76. Immunodefic Rev. 1992. PMID: 1449786 Review.
Cited by
- Identification of CD160-TM as a tumor target on triple negative breast cancers: possible therapeutic applications.
Scheffges C, Devy J, Giustiniani J, Francois S, Cartier L, Merrouche Y, Foussat A, Potteaux S, Bensussan A, Marie-Cardine A. Scheffges C, et al. Breast Cancer Res. 2024 Feb 15;26(1):28. doi: 10.1186/s13058-024-01785-x. Breast Cancer Res. 2024. PMID: 38360636 Free PMC article. - Experimental and phylogenetic evidence for correlated gene expression evolution in endometrial and skin fibroblasts.
Dighe A, Maziarz J, Ibrahim-Hashim A, Gatenby RA, Kshitiz, Levchenko A, Wagner GP. Dighe A, et al. iScience. 2023 Nov 29;27(1):108593. doi: 10.1016/j.isci.2023.108593. eCollection 2024 Jan 19. iScience. 2023. PMID: 38174318 Free PMC article. - Establishment of anti-asialo-GM1 rabbit monoclonal antibodies capable of reducing natural killer cell activity in mice.
Kimura T, Ohta S, Murayama H. Kimura T, et al. PLoS One. 2023 Oct 9;18(10):e0292514. doi: 10.1371/journal.pone.0292514. eCollection 2023. PLoS One. 2023. PMID: 37812617 Free PMC article. - Murine models to study human NK cells in human solid tumors.
Parodi M, Astigiano S, Carrega P, Pietra G, Vitale C, Damele L, Grottoli M, Guevara Lopez ML, Ferracini R, Bertolini G, Roato I, Vitale M, Orecchia P. Parodi M, et al. Front Immunol. 2023 Jun 14;14:1209237. doi: 10.3389/fimmu.2023.1209237. eCollection 2023. Front Immunol. 2023. PMID: 37388731 Free PMC article. Review. - IL-15 Prevents the Development of T-ALL from Aberrant Thymocytes with Impaired DNA Repair Functions and Increased NOTCH1 Activation.
Nandi M, Ghosh A, Akbari SA, Bobbala D, Boucher MJ, Menendez A, Hoang T, Ilangumaran S, Ramanathan S. Nandi M, et al. Cancers (Basel). 2023 Jan 21;15(3):671. doi: 10.3390/cancers15030671. Cancers (Basel). 2023. PMID: 36765626 Free PMC article.
Publication types
MeSH terms
LinkOut - more resources
Full Text Sources
Other Literature Sources