TRANSPLANTATION OF THYMIC TISSUE IN INBRED STRAINS OF MICE

1961 ◽  
Vol 22 (4) ◽  
pp. 349-359 ◽  
Author(s):  
FLORENCE J. PEPPER
Keyword(s):  
Lymph Nodes ◽  
Adrenal Glands ◽  
Inbred Strains ◽  
Body Growth ◽  
Thymus Gland ◽  
Thymic Tissue ◽  
Adrenocortical Hormones ◽  
Loss Of Weight ◽  
Inbred Strains Of Mice ◽  
Different Ages

SUMMARY Thymic tissue has been transplanted between donor and host mice of different ages. It has been found that thymic tissue more than a few days old loses weight rapidly when transplanted to a host, and that beyond this age loss of weight is independent of the age of either donor or host. For the first few days after birth the thymus gland is capable of growth when transplanted to a host and, unlike the host's own thymus, it is unaffected by the increased output of adrenocortical hormones which occurs during pregnancy. The behaviour of a thymic graft seems to be independent of the presence or absence of the host's own thymus gland. The presence of additional thymic tissue in a host appears to have no effect on body growth, weight of adrenal glands, gonads and superficial lymph nodes, or on the weight and histological condition of the thymus of the host.

Effects of Foster Nursing on Alcohol Selection in Inbred Strains of Mice

1972 ◽  
Vol 33 (2) ◽  
pp. 494-503 ◽  
Author(s):  
Setsuo Komura ◽  
Masao Ueda ◽  
Toshikiyo Kobayashi
Keyword(s):  
Inbred Strains ◽  
Inbred Strains Of Mice

Duplications and deletions of Vh genes in inbred strains of mice

1988 ◽  
Vol 28 (2) ◽  
pp. 125-135 ◽  
Author(s):  
Adele Tutte ◽  
Roy Riblet
Keyword(s):  
Inbred Strains ◽  
Inbred Strains Of Mice ◽  
Vh Genes

scholarly journals THE GENETIC DIVERGENCE OF SUBLINES AS ASSESSED BY HISTOCOMPATIBILITY TESTING

Genetics ◽  
1973 ◽  
Vol 75 (4) ◽  
pp. 671-677
Author(s):  
Willys K Silvers ◽  
David L Gasser
Keyword(s):  
Genetic Divergence ◽  
Inbred Strains ◽  
Skin Grafts ◽  
Inbred Strains Of Mice ◽  
Inbred Rats

ABSTRACT The degree of genetic divergence which has occurred between a number of inbred strains of mice and between two sublines of inbred rats was assessed by determining the fate of inter-subline skin grafts. Sublines which had been separated for 29 and 42 generations possessed no detectable incompatibility, while three combinations of sublines judged to have been maintained apart for from 123 to 129 generations showed slight degrees of histoincompatibility. One pair of sublines which had been separated for 119 generations demonstrated a marked degree of incompatibility, and an F2 test suggested that mutations had occurred at four or five histocompatibility loci.

scholarly journals A new allele of the lpr locus, lprcg, that complements the gld gene in induction of lymphadenopathy in the mouse.

1990 ◽  
Vol 171 (2) ◽  
pp. 519-531 ◽  
Author(s):  
A Matsuzawa ◽  
T Moriyama ◽  
T Kaneko ◽  
M Tanaka ◽  
M Kimura ◽  
...  
Keyword(s):  
Recessive Gene ◽  
Mutant Gene ◽  
Inbred Strains ◽  
Lymphoid Hyperplasia ◽  
Lymphoid Cells ◽  
Autoantibody Production ◽  
Genetic Studies ◽  
Inbred Strains Of Mice ◽  
Backcross Populations ◽  
Generalized Lymphadenopathy

Several mice with generalized lymphadenopathy were found in the CBA/KlJms (CBA) colony maintained at our institute. A new mutant strain of mice that develop massive lymphoid hyperplasia at 100% incidence within 5 mo after birth was established by crossing these diseased mice. Genetic studies on lymphadenopathy were conducted in F1, F2, and backcross populations from crosses between mutant CBA (CBA-m) and various inbred strains of mice. The results supported the control of lymphadenopathy by a single autosomal recessive gene. Since C3H/He-gld/gld (C3H-gld), MRL/MpJ-lpr/lpr (MRL-lpr), and C3H/HeJ-lpr/lpr (C3H-lpr) mice develop the same type of lymphoid hyperplasia, allelism of the mutant gene with gld or lpr was tested by investigating lymphadenopathy in F1 and backcross populations from crosses between CBA-m and C3H-gld, MRL-lpr, or C3H-lpr mice. The gene was confirmed to be allelic with lpr but not with gld. Interestingly, however, the mutant gene interacted with gld to induce less severe lymphadenopathy. Thus, the mutant gene was named lprcg, an lpr gene complementing gld in induction of lymphoproliferation. The genetic conclusion was supported by the same profile of surface markers of lymphoid cells with gld/gld, lpr/lpr, lprcg/lprcg, lprcg/lpr, and +/gld +/lprcg genotypes, as well as by massive lymph node hyperplasia and high titers of autoantibodies in the first four genotypes, but slight hyperplasia and insignificant autoantibody production in the last. The discovery of lprcg provided strong genetic evidence for the parallels between anomalous phenotypes of gld and lpr, and CBA/KlJms-lprcg/lprcg mice will contribute to elucidation of the mechanism of induction of the same abnormal differentiation and functions of lymphocytes by gld and lpr.

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