Literature DB >> 6333455

Aberrant expression of Forssman and Paul-Bunnell antigens on lymph node cells of MRL/Mp-lpr/lpr mice.

T Katagiri, T Mori, T Nakano, K Ueno, K Kano.   

Abstract

Lymph node cells (LNC) of MRL/Mp-lpr/lpr mice (MRL/1) and congeneic MRL/Mp-+/+ (MRL/n) mice were studied by means of flow fluorocytometry for the expression of heterophile Forssman (F) and Paul-Bunnell (P-B) antigens. The level of F antigen on LNC of MRL/1, but not on those of MRL/n mice, increased progressively with age and reached its maximum at 4 mo of age. No such increase in F antigen on LNC of age-matched C3H/HeJms, C57BL/6, and AKR mice was observed. In contrast, the level of P-B antigen on LNC of MRL/1 mice was significantly lower than that of MRL/n and the normal mice. F-positive LNC of MRL/1 mice were shown to be T cells with Thy-1.2 and Lyt-1 markers; those cells expanded in the lymph nodes and were responsible for the development of the massive lymphadenopathy. Studies on LNC of F1 hybrids between MRL/1 and MRL/n mice, and animals of the subsequent F2 generation provided evidence that the aberrant expression of F and P-B antigens was under the influence of the autosomal recessive lpr gene and was segregated together with the lymphadenopathy into the F2 generation. The aberrant expression of F and P-B antigens reflects the alteration of terminal carbohydrate structure of glycolipids and glycoproteins on the membrane of the LNC. It is tempting, therefore, to speculate that such alterations in the membrane structure might represent disturbances in cellular recognition resulting in unusual expansion of the T cells in the early life of MRL/1 mice.

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Year:  1984        PMID: 6333455

Source DB:  PubMed          Journal:  J Immunol        ISSN: 0022-1767            Impact factor:   5.422


  6 in total

1.  Lung lymphocyte elimination by apoptosis in the murine response to intratracheal particulate antigen.

Authors:  A M Milik; V A Buechner-Maxwell; J Sonstein; S Kim; G D Seitzman; T F Beals; J L Curtis
Journal:  J Clin Invest       Date:  1997-03-01       Impact factor: 14.808

2.  Agalactosyl IgG and beta-1,4-galactosyltransferase gene expression in rheumatoid arthritis patients and in the arthritis-prone MRL lpr/lpr mouse.

Authors:  P A Jeddi; K B Bodman-Smith; T Lund; P M Lydyard; L Mengle-Gaw; D A Isenberg; P Youinou; P J Delves
Journal:  Immunology       Date:  1996-04       Impact factor: 7.397

3.  Reduced galactosyltransferase mRNA levels are associated with the agalactosyl IgG found in arthritis-prone MRL-lpr/lpr strain mice.

Authors:  P A Jeddi; T Lund; K B Bodman; N Sumar; P M Lydyard; L Pouncey; L S Heath; V J Kidd; P J Delves
Journal:  Immunology       Date:  1994-11       Impact factor: 7.397

4.  The lpr gene causes an intrinsic T cell abnormality that is required for hyperproliferation.

Authors:  T Katagiri; P L Cohen; R A Eisenberg
Journal:  J Exp Med       Date:  1988-03-01       Impact factor: 14.307

5.  Crosstalk between ABO and Forssman (FORS) blood group systems: FORS1 antigen synthesis by ABO gene-encoded glycosyltransferases.

Authors:  Miyako Yamamoto; Emili Cid; Fumiichiro Yamamoto
Journal:  Sci Rep       Date:  2017-01-30       Impact factor: 4.379

Review 6.  Association of lpr gene with graft-vs.-host disease-like syndrome.

Authors:  A N Theofilopoulos; R S Balderas; Y Gozes; M T Aguado; L M Hang; P R Morrow; F J Dixon
Journal:  J Exp Med       Date:  1985-07-01       Impact factor: 14.307

  6 in total

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