AI Article Synopsis
Article Abstract
The functional differences between two mutations of the Fas (CD95) locus, Faslpr (lpr) and Faslprcg (lprcg), were investigated using bone marrow (BM) transplantation on the C3H mouse background. Both lpr/lpr and lprcg/lprcg BM transferred caused lymph node (LN) hyperplasia in lpr/+ and lprcg/+ recipients, although it was clearly smaller than that in lpr/lpr and lprcg/lprcg recipients of lpr/lpr and lprcg/lprcg BM. In addition, both BM induced significantly larger LN hyperplasia in lprcg/+ than lpr/+ recipients. Appearance of CD4- CD8-[double negative (DN)] T cells in the periphery is the most consistent phenotype of Fas mutations. Importantly, the proportion of DN T cells was higher in larger LN hyperplasia in the order of lpr/+, lprcg/+ and lpr/lpr or lprcg/lprcg recipients. On the other hand, both lpr/lpr and lprcg/lprcg BM transferred into wild-type (+/+) mice caused marked LN atrophy. The former, but not the latter, induced wasting syndrome. Faslg1d (gld)-homozygous lpr/lpr BM transferred into +/+ mice elicited LN hyperplasia of the same extent as that in lpr/lpr mice transferred with lpr/lpr BM, but not wasting syndrome. Taken together with the fact that DN T cells massively express Fas ligand (FasL), this study implied that FasL overexpressed on DN cells may be involved in the accumulation of DN T cells in LN, LN atrophy and wasting syndrome, and that lprcg Fas, which can bind to Fas ligand but not transduce apoptosis signal into cells, may modulate these pathological conditions by interfering with the binding of FasL to Fas.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1782754 | PMC |
| http://dx.doi.org/10.1046/j.1365-2567.2002.01462.x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Significant role of Fas ligand-binding but defective Fas receptor (CD95) in lymph node hyperplasia composed of abnormal double-negative T cells.
Immunology
August 2002
Laboratory Animal Research Center and Department of Surgery, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo, Metropolitan Institute of Medical Science, Honkomagome, Bunkyo-ku, Tokyo, Japan.
The functional differences between two mutations of the Fas (CD95) locus, Faslpr (lpr) and Faslprcg (lprcg), were investigated using bone marrow (BM) transplantation on the C3H mouse background. Both lpr/lpr and lprcg/lprcg BM transferred caused lymph node (LN) hyperplasia in lpr/+ and lprcg/+ recipients, although it was clearly smaller than that in lpr/lpr and lprcg/lprcg recipients of lpr/lpr and lprcg/lprcg BM. In addition, both BM induced significantly larger LN hyperplasia in lprcg/+ than lpr/+ recipients.
View Article and Find Full Text PDFStudies on the mechanism of dimethylnitrosamine-induced acute liver injury in mice.
Exp Toxicol Pathol
December 1997
Department of Pathology, Kansai Medical University, Osaka, Japan.
Male and female adult C3H- +/+, C3H-gld/gld.lpr/lpr (gld.lpr) and CBA-lprcg/lprcg (lprcg) mice were given a single i.
View Article and Find Full Text PDFFas-independent apoptosis of photoreceptor cells in C3H mice.
Exp Anim
October 1996
Department of Ophthalmology, Kansai Medical University, Osaka, Japan.
The morphogenesis of the photoreceptor cells in the retinas of C3H mice carrying the rd gene and C57BL mice carrying the normal gene was compared, and retinas of the C3H mutants (C3H-lpr/lpr, -lprcg/lprcg, and -lpr/lpr-gld/gld) defective in apoptosis through the Fas system were examined. In the C57BL retina, the inner and outer nuclear layers were separated at 8 days of age, and the photoreceptor inner and outer segments began to grow between 8-11 days after birth with their most rapid growth occurring between 14-17 days of age. In the C3H retina, the development was comparable to that of the C57BL retina at 8 days of age but the reduction in thickness of the outer nuclear and photoreceptor layers was noted at 11 days of age, and the outer nuclear layer became reduced to only a few nuclei in thickness at 14 days, being completely missing or reduced to a single row of cells at 20 days.
View Article and Find Full Text PDFLymphadenopathy induced by the cooperation between lprcg and gld genes is of lpr but not of gld phenotype.
Eur J Immunol
July 1994
Laboratory Animal Research Center, University of Tokyo, Japan.
Mice homozygous for the lpr (lymphoproliferation), lprcg or gld (generalized lymphoproliferative disease) mutation develop strikingly similar lymphadenopathy with expansion of B220+ CD4- CD8- double-negative (DN) T cells and autoimmunity. To elucidate the roles of bone marrow (BM) and lymph node (LN) in lymphoproliferation, BM and LN were transplanted simultaneously into normal or +/+ mice in various genotype combinations. In lpr/lpr or lprcg/lprcg BM recipients grafted lpr/lpr and lprcg/lprcg LN swelled but +/+ and gld/gld LN atrophied.
View Article and Find Full Text PDFAutoimmunity in mice bearing lprcg: a novel mutant gene.
Int Rev Immunol
October 1994
Department of Infectious Diseases and Applied Immunology, University of Tokyo, Japan.
A novel mutation at the lpr (lymphoproliferation)(Fas) locus, lprcg, that can complement gld (generalized lymphoproliferative disease) in induction of lymphadenopathy was discovered in CBA/K1Jms mice. The lpr and lprcg mutations are a defective allele of the Fas locus that encodes an apoptosis-mediating receptor. The former does not express the receptor and the latter expresses the point-mutated nonfunctional receptor.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!