scholarly journals Modulation of multiple experimental arthritis models by collagen-induced arthritis quantitative trait loci isolated in congenic rat lines: Different effects of non-major histocompatibility complex quantitative trait loci in males and females

2002 ◽  
Vol 46 (8) ◽  
pp. 2225-2234 ◽  
Author(s):  
Elaine F. Remmers ◽  
Bina Joe ◽  
Marie M. Griffiths ◽  
David E. Dobbins ◽  
Svetlana V. Dracheva ◽  
...  
1997 ◽  
Vol 70 (2) ◽  
pp. 117-124 ◽  
Author(s):  
KELLIE A. RANCE ◽  
WILLIAM G. HILL ◽  
PETER D. KEIGHTLEY

Evidence of a large sex-linked effect accounting for 25% of the divergence between mouse lines selected for body weight has been described previously. A marker-based study was undertaken to determine the number and map positions of the putative X-linked quantitative trait loci (QTLs). An F2 population was generated from a reciprocal F1 between an inbred low line derived from the low selection line and the high selection line. To enable inference of marker-associated QTL effects on the X chromosome, an analytical technique was developed based on the multiple regression method of Haley and Knott. The analysis of data on 10 week weight indicated a single QTL of large effect situated at about 23 cM from the proximal end of the chromosome, with a peak LOD score of 24·4. The likelihood curve showed a single well-defined peak, and gave a 95% confidence interval for the QTL location of 8 cM. The estimates for the additive genotypic effects in males and females (half the differences between hemizygous males and between homozygous females) were 2·6 g in both cases, or 17% and 20% of the 10 week body weight in males and females respectively. Dominance effects in the females were found to be non-significant. No significant X-linked effect on carcass fat percentage was detected, but a single X-linked QTL appears to explain almost the entire X-linked body weight effect.


2002 ◽  
Vol 80 (3) ◽  
pp. 225-230 ◽  
Author(s):  
SARAH G. REIWITCH ◽  
SERGEY V. NUZHDIN

The properties of alleles at quantitative trait loci (QTLs) contributing to variation in lifespan should be described to determine the mechanisms of evolution of life length and to predict its future changes. Previously, we and others conducted genome-wide screens for QTLs that segregate among one panel of recombinant inbred lines (RILs) using a dense molecular marker map. In non-stressful conditions, QTLs effecting the lifespans of virgin females and males were frequently sex specific. In an unrelated panel of RILs, the effects of QTLs in flies maintained in cages with mixed sexes were similar in both sexes. Here, we re-measured the lifespans of the former panel of RILs in cages with mixed sex cohorts. Lifespan declined owing to mating. The amount of decline correlated between sexes within lines. QTLs mapping to the intervals 15A–19C, 50B–57C, 63A–65A, and 96F–99B had similar effects on the lifespans of both males and females. These QTLs have previously been detected in virgin flies surveys and had sex- and/or environment-specific effects.


1992 ◽  
Vol 175 (4) ◽  
pp. 933-937 ◽  
Author(s):  
N P Bakker ◽  
M G van Erck ◽  
N Otting ◽  
N M Lardy ◽  
R C Noort ◽  
...  

Type II collagen-induced arthritis (CIA) is an experimentally inducible autoimmune disorder that is, just like several forms of human arthritis, influenced by a genetic background. Immunization of young rhesus monkeys (Macaca mulatta) with type II collagen (CII) induced CIA in about 70% of the animals. One major histocompatibility complex (MHC) class I allele was present only in young animals resistant to CIA and absent in arthritic animals. This strong association suggests that the MHC class I allele itself, or a closely linked gene, determines resistance to CIA. The mechanism controlling the resistance to CIA becomes less efficient in aged animals since older rhesus monkeys, which were positive for the resistance marker, developed a mild form of arthritis. At the cellular level it is demonstrated that resistance to CIA is reflected by a low responsiveness of T cells to CII. This association between a specified MHC class I allele and resistance to an autoimmune disease points at the importance of the MHC class I region in the regulation of the immune response to an autoantigen.


2018 ◽  
Vol 285 (1884) ◽  
pp. 20180841 ◽  
Author(s):  
Jacob Roved ◽  
Bengt Hansson ◽  
Maja Tarka ◽  
Dennis Hasselquist ◽  
Helena Westerdahl

Sex differences in parasite load and immune responses are found across a wide range of animals, with females generally having lower parasite loads and stronger immune responses than males. Intrigued by these general patterns, we investigated if there was any sign of sex-specific selection on an essential component of adaptive immunity that is known to affect fitness, the major histocompatibility complex class I (MHC-I) genes, in a 20-year study of great reed warblers. Our analyses on fitness related to MHC-I diversity showed a highly significant interaction between MHC-I diversity and sex, where males with higher, and females with lower, MHC-I diversity were more successful in recruiting offspring. Importantly, mean MHC-I diversity did not differ between males and females, and consequently neither sex reached its MHC-I fitness optimum. Thus, there is an unresolved genetic sexual conflict over MHC-I diversity in great reed warblers. Selection from pathogens is known to maintain MHC diversity, but previous theory ignores that the immune environments are considerably different in males and females. Our results suggest that sexually antagonistic selection is an important, previously neglected, force in the evolution of vertebrate adaptive immunity, and have implications for evolutionary understanding of costs of immune responses and autoimmune diseases.


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