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. 1974 May 1;139(5):1142–1153. doi: 10.1084/jem.139.5.1142

ONTOGENY OF B LYMPHOCYTES

III. H-2 LINKAGE OF A GENE CONTROLLING THE RATE OF APPEARANCE OF COMPLEMENT RECEPTOR LYMPHOCYTES

Michael C Gelfand 1, David H Sachs 1, Rose Lieberman 1, William E Paul 1
PMCID: PMC2139659  PMID: 4545163

Abstract

The frequency of lymphocytes bearing complement receptors in the spleens of 2-wk old mice appears to be controlled by two independent genes. The presence of a "high" allele at either locus leads to intermediate or high frequency of CRL at 2 wk of age. One of the genes controlling complement receptor lymphocyte (CRL) frequency (CRL-1) is linked to the H-2 complex. Thus, in progeny of (AKR x DBA/2)F1 x DBA/2, all mice with a low frequency of CRL at 2 wk of age are homozygous for the H-2 type of the low CRL parent (DBA/2). Furthermore, in the B10 series of congenic mice, CRL frequency at 2 wk of age is similar to the frequency in the donor of the H-2 region. Thus, C57BL/10, B10.BR, and B10-D2 mice are all of the low CRL type while B10.A mice are intermediate in CRL frequency at 2 wk. C57BR and DBA/2, the donors of the H-2 complex of the B10.BR and B10.D2, respectively, are of low CRL type while the A/WySn, the donor of the H-2 complex in the B10.A, is an intermediate CRL strain. Similarly in the A/WySn series of congenic mice, A.CA, A.SW, and A.BY are all low CRL strains while the A/WySn is intermediate. Studies of CRL frequency in mice with recombinant H-2 chromosomes (B10.A(2R), (4R), and (5R); B6/TL+; and A/TL-) indicate that CRL-1 is to the right of the Ss-Slp genes and to the left of Tla.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Amsbaugh D. F., Hansen C. T., Prescott B., Stashak P. W., Barthold D. R., Baker P. J. Genetic control of the antibody response to type 3 pneumococcal polysaccharide in mice. I. Evidence that an X-linked gene plays a decisive role in determining responsiveness. J Exp Med. 1972 Oct 1;136(4):931–949. doi: 10.1084/jem.136.4.931. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Bach F. H., Widmer M. B., Bach M. L., Klein J. Serologically defined and lymphocyte-defined components of the major histocompatibility complex in the mouse. J Exp Med. 1972 Dec 1;136(6):1430–1444. doi: 10.1084/jem.136.6.1430. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Bianco C., Patrick R., Nussenzweig V. A population of lymphocytes bearing a membrane receptor for antigen-antibody-complement complexes. I. Separation and characterization. J Exp Med. 1970 Oct 1;132(4):702–720. doi: 10.1084/jem.132.4.702. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. David C. S., Shreffler D. C., Frelinger J. A. New lymphocyte antigen system (Lna) controlled by the Ir region of the mouse H-2 complex. Proc Natl Acad Sci U S A. 1973 Sep;70(9):2509–2514. doi: 10.1073/pnas.70.9.2509. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Démant P., Capková J., Hinzová E., Vorácová B. The role of the histocompatibility-2-linked Ss-Slp region in the control of mouse complement. Proc Natl Acad Sci U S A. 1973 Mar;70(3):863–864. doi: 10.1073/pnas.70.3.863. [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Götze D., Reisfeld R. A., Klein J. Serologic evidence for antigens controlled by the Ir region in mice. J Exp Med. 1973 Oct 1;138(4):1003–1008. doi: 10.1084/jem.138.4.1003. [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Hauptfeld V., Klein D., Klein J. Serological identification of an Ir-region product. Science. 1973 Jul 13;181(4095):167–169. doi: 10.1126/science.181.4095.167. [DOI] [PubMed] [Google Scholar]
  8. Katz D. H., Hamaoka T., Dorf M. E., Maurer P. H., Benacerraf B. Cell interactions between histoincompatible T and B lymphocytes. IV. Involvement of the immune response (Ir) gene in the control of lymphocyte interactions in responses controlled by the gene. J Exp Med. 1973 Sep 1;138(3):734–739. doi: 10.1084/jem.138.3.734. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Klein J., Shreffler D. C. Evidence supporting a two-gene model for the H-2 histocompatibility system of the mouse. J Exp Med. 1972 Apr 1;135(4):924–937. doi: 10.1084/jem.135.4.924. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Klein J. The H-2 system: past and present. Transplant Proc. 1973 Mar;5(1):11–21. [PubMed] [Google Scholar]
  11. LIEBERMAN R., DRAY S. FIVE ALLELIC GENES AT THE ASA LOCUS WHICH CONTROL GAMMA-GLOBULIN ALLOTYPIC SPECIFICITIES IN MICE. J Immunol. 1964 Oct;93:584–594. [PubMed] [Google Scholar]
  12. Lieberman R., Paul W. E., Humphrey W., Jr, Stimpfling J. H. H-2-linked immune response (Ir) genes. Independent loci for Ir-IgG and Ir-IgA genes. J Exp Med. 1972 Nov 1;136(5):1231–1240. doi: 10.1084/jem.136.5.1231. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. McDevitt H. O., Deak B. D., Shreffler D. C., Klein J., Stimpfling J. H., Snell G. D. Genetic control of the immune response. Mapping of the Ir-1 locus. J Exp Med. 1972 Jun 1;135(6):1259–1278. doi: 10.1084/jem.135.6.1259. [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Sachs D. H., Cone J. L. A mouse B-cell alloantigen determined by gene(s) linked to the major histocompatibility complex. J Exp Med. 1973 Dec 1;138(6):1289–1304. doi: 10.1084/jem.138.6.1289. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Sachs D. H., Winn H. J., Russell P. S. The immunologic response to xenografts. Recognition of mouse H-2 histocompatibility antigens by the rat. J Immunol. 1971 Aug;107(2):481–492. [PubMed] [Google Scholar]
  16. Shevach E. M., Rosenthal A. S. Function of macrophages in antigen recognition by guinea pig T lymphocytes. II. Role of the macrophage in the regulation of genetic control of the immune response. J Exp Med. 1973 Nov 1;138(5):1213–1229. doi: 10.1084/jem.138.5.1213. [DOI] [PMC free article] [PubMed] [Google Scholar]

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