Immunology Today. Vol. I l. No. 12 1990
!0, 313-315), it is unlikely that an allele of the Thy-1 gene itself is responsible for AT. In a letter to the editor (Immunol. Today, 1 I, 230), Marian Laderoute has suggested that Sir° Ataxia telangiectasia (AT) is an the ets-I gene, also located in the autosomal recessive disorder 1 Iq22-23 region, is a promising cancharacterized by a wide range of didate for the AT gene. Using the same set of AT families in developmental and immunological abnormalities including cerebellar which linkage to Fhy-I was originally ataxia, radiation sensitivity, immuno- demonstrated and a restriction fragdeficiency, chromosomal instability ment length polymorphisrn (RFLP)deand an increased incidence of cancer. tected with an ets-I gene probe, we A gene for AT has been localized to have specifically tested the hypoththe chromosoma! region 1 lq22-23 esis that an allele of ets-1 may be by qenetic linkage to the gene for responsible for AT2. Our linkage Thy-1 (Ref. 1). As Raymond Peterson analysis places the ets-I gene apand Jane Funkhouser correctly proximately 19 centimorgans telopointed out (irnmunoL Today. 1989, meric to Thy-1 and excludes an AT
The ets-1 gene and ataxia telangiectasia
?.xpression of CD45 on T-cell populations Sir, In the article 'Limiting dilution analysis of human T cells: a useful clinical tool" by C. Sharrock et aL (Immunol. loday. 1990, 11, 281-286), the authors discuss the evidence for precursor populations. However, although the essence of the argument is correct, the description of the exv,
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concerned is completely wrong. CD45 is expressed on all leuco@tes and it is the expression of its isoforms which differentiates between the CD4 + subsets. The population with low trequ~ncy of tetanus toxoid re-
sponding cells expresses the heavy molecular weight isoforms requiring expression of exon A at the 5' end of the CD45 gene and is termed CD45RA +. The population that is enriched for recall antigen-specific resp~nders expresses the low molecular weight isoform, CD45RO, generated by splicing out exons A, B and C and does not express the CD45RA isoformsl. 2. Moreover, the CD45RA phenotype of CD8 + cytotoxic T cells has been charaC,t,rized in humans using Epstein-Barr virus (EBV)-transformed cell lines3 and in the mouse using Kbtransfected cell lines by our group 4. The CD nomenclature in general and that of CD45 and its isoforms in particular is already complicated.
gene from a region extending 15 centimorgans to either side of the ets- 1 gene. These data effectively exclude ets- 1 as a candk ate for the AT gene and strongly su!ig6st that any additional candi0at~ ~i~ould be drawn from those genes that are located ce~tron,::,-ic to Thy- 1.
Patrick Concannon Virginia MasonResearchCenter, Seattle, WA 98101, USA.
References 1 Gatti, R ~,., BerLel, I., Boder, E. et al. (1988) Nature 336, 577-580 2 Concannon, P., Malhotra, U., Charmley, P. et al. (1990)Am. J. Hum. Genet. 46, 789-794
We, therefore, feei that it is imperative, particularly in review articles, that it is used accurately.
Elizabeth Lightstone Jacqueline Marvel ICRFTurnour Immunology U~fit Dept of Biology, UniversityCollege, London WC1E 6BT, UK.
References 1 k:erkenschlager, M., Terry,,L., Edwards, R. et al. (1988) ~ur. J. Immunol. 18, 1653-i66i 2 Streuli, M., Morimoto, C., Schrieber, M. et aL (1988)J. Immunol. 141, 3910-3914 3 Merkenschlager, M. and Beverley, P.C. (1989) Int. ImmunoL 1,450-459 4 Marvel, J., Lightstone, E.B., Samberg, N.L et aL Int. Immunol. (in press)
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