| Literature DB >> 35690417 |
Noah A Kaitz1, Cindy L Zuleger2, Peng Yu3, Michael A Newton4, Richard J Albertini5, Mark R Albertini6.
Abstract
Somatic cell gene mutations arise in vivo due to replication errors during DNA synthesis occurring spontaneously during normal DNA synthesis or as a result of replication on a DNA template damaged by endogenous or exogenous mutagens. In principle, changes in the frequencies of mutant cells in vivo in humans reflect changes in exposures to exogenous or endogenous DNA damaging insults, other factors being equal. It is becoming increasingly evident however, that somatic mutations in humans have a far greater range of interpretations. For example, mutations in lymphocytes provide invaluable probes for in vivo cellular and molecular processes, providing identification of clonal amplifications of these cells in autoimmune and infectious diseases, transplantation recipients, paroxysmal nocturnal hemoglobinuria (PNH), and cancer. The assay for mutations of the X-chromosomal hypoxanthine guanine phosphoribosyltransferase (HPRT) gene has gained popular acceptance for this purpose since viable mutant cells can be recovered for molecular and other analyses. Although the major application of the HPRT T cell assay remains human population monitoring, the enrichment of activated T cells in the mutant fraction in individuals with ongoing immunological processes has demonstrated the utility of surrogate selection, a method that uses somatic mutation as a surrogate marker for the in vivo T cell proliferation that underlies immunological processes to investigate clinical disorders with immunological features. Studies encompassing a wide range of clinical conditions are reviewed. Despite the historical importance of the HPRT mutation system in validating surrogate selection, there are now additional mutational and other methods for identifying immunologically active T cells. These methods are reviewed and provide insights for strategies to extend surrogate selection in future studies.Entities:
Keywords: Hypoxanthine Guanine Phosphoribosyltransferase gene; Phosphoinositolglycan class A gene; Spontaneous T cell gene mutations; Surrogate selection
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Year: 2022 PMID: 35690417 PMCID: PMC9188651 DOI: 10.1016/j.mrrev.2022.108414
Source DB: PubMed Journal: Mutat Res Rev Mutat Res ISSN: 1383-5742 Impact factor: 7.015