Genetic analyses of alloreactions between recently wild and classical inbred strains of syrian hamsters: Evidence in favor of a major histocompatibility complex

1981 ◽  
Vol 13 (5) ◽  
pp. 393-403 ◽  
Author(s):  
William R. Duncan ◽  
J. Wayne Streilein
Keyword(s):  
Major Histocompatibility Complex ◽  
Inbred Strains ◽  
Major Histocompatibility ◽  
Genetic Analyses ◽  
Syrian Hamsters ◽  
Histocompatibility Complex

scholarly journals Recognition among mice. Evidence from the use of a Y-maze differentially scented by congenic mice of different major histocompatibility types.

1979 ◽  
Vol 150 (4) ◽  
pp. 755-760 ◽  
Author(s):  
K Yamazaki ◽  
M Yamaguchi ◽  
L Baranoski ◽  
J Bard ◽  
E A Boyse ◽  
...  
Keyword(s):  
Sex Differences ◽  
Major Histocompatibility Complex ◽  
Water Deprivation ◽  
Inbred Strains ◽  
The Other ◽  
Major Histocompatibility ◽  
Male And Female ◽  
Sensory Discrimination ◽  
Histocompatibility Complex ◽  
Y Maze

Previous studies of mating preference signified that mice can sense one another's major histocompatibility complex (MHC) types, probably by olfaction. This conclusion has now been substantiated by the use of a Y-maze whose two arms were differentially scented with currents of air conducted through boxes occupied by B6 (H-2b) males and by B6-H-2k congenic males. Four B6 mice, two males and two females, were successfully trained, by water deprivation and reward, to enter the arm scented by B6 or B6-H-2k males. One of the males and one of the females were trained to select the B6-scented arm; the other male and female were trained to select the B6-H-2k-scented arm. Untrained mice showed no MHC discrimination in the maze. The performance of the trained mice in distinguishing between MHC congenic homozygous F2 segregants derived from a cross of B6-H-2k with B6 was as good as their performance in distinguishing the respective inbred strains, thus essentially eliminating alternative and significant additional explanations of MHC-associated sensory discrimination. The data further indicate that chemosensory discrimination of MHC types can be entirely dissociated from sex differences and from the circumstances of mating.

scholarly journals Genetic susceptibility to murine collagen II autoimmune arthritis. Proposed relationship to the IgG2 autoantibody subclass response, complement C5, major histocompatibility complex (MHC) and non-MHC loci.

1985 ◽  
Vol 162 (6) ◽  
pp. 1878-1891 ◽  
Author(s):  
W C Watson ◽  
A S Townes
Keyword(s):  
Major Histocompatibility Complex ◽  
Inbred Strains ◽  
Autoimmune Response ◽  
F1 Hybrids ◽  
Autoimmune Arthritis ◽  
Major Histocompatibility ◽  
F1 Hybrid ◽  
Histocompatibility Complex ◽  
Autoantibody Response ◽  
Collagen Ii

Analysis of the IgG autoantibody subclass response in the collagen II autoimmune arthritis (CII AIA)-susceptible D1 strain mice revealed that the onset of disease was associated with a predominance of IgG2a autoantibody. In a comparative study, resistance in the B6 strain was associated with a deficient IgG2a autoantibody response. B6 IgG1, 2b, and 3 autoantibody responses generally overlapped those of arthritic D1 mice, and estimates of antibody crossreactivity and affinity were similar for both strains. In crosses between D1 and B6, arthritis developed only in those F1 mice with IgG2a autoantibody responses approximating or exceeding those in arthritic D1 mice. Additional studies with B6 and B10 strains suggested an alternate role for the IgG2b autoantibody response. In inbred strains with known genetic backgrounds, a dissociation between the magnitude of the total IgG autoantibody response and the percent of total as IgG2a was demonstrated. The H-2q, Ig-1c D1 strain was a high-total and high-percent IgG2a responder, while the H-2d, Ig-1c D2 strain was a low-total but high-percent IgG2a responder. The H-2b, Ig-1b B6 strain was a low-total and low-percent IgG2a responder, while the H-2b/q, Ig-1b/c (B6D1)F1 hybrid was a low-total but high-percent IgG2a responder. A further dissociation between high-percent IgG2a autoantibody responsiveness and the H-2 haplotype was demonstrated by the H-2 congenic B10.D2/n (H-2d, Ig-1b) strain, in which a low-percent IgG2a response was observed to differ from the D2 strain. High-percent IgG2a autoantibody responsiveness also appeared to be inherited as a dominant trait based upon high responses in all (B6D1)F1 hybrids and backcrosses to D1. These findings suggest that the H-2 haplotype is involved in the total IgG autoantibody response but that the relative fraction of the total response as IgG2a is independent of the H-2 haplotype and possibly related to Igh-C genes. C5-deficient SWR (H-2q, Ig-1c) mice were found to have a high total autoantibody response to mouse CII and IgG2a comparable to arthritic D1 mice, but these mice did not develop arthritis. Based upon these observations, we conclude that susceptibility to CII AIA requires the interaction of multiple genes, both major histocompatibility complex (MHC) and non-MHC, which influence the magnitude (total IgG) and the quality (IgG subclass) of the autoimmune response and the availability of appropriate mediators (C5) to initiate the inflammatory reaction.

Immunobiology of neural transplants and functional incorporation of grafted dopamine neurons

1995 ◽  
Vol 18 (1) ◽  
pp. 48-49
Author(s):  
Jeffrey B. Blount ◽  
Takeshi Kondoh ◽  
Lisa L. Pundt ◽  
John Conrad ◽  
Elizabeth M. Jansen ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Experimental Work ◽  
Inbred Strains ◽  
Dopamine Neurons ◽  
Immune Rejection ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Transplantation Immunology ◽  
Neural Transplants

AbstractIn contrast to the views put forth by Stein & Glasier, we support the use of inbred strains of rodents in studies of the immunobiology of neural transplants. Inbred strains demonstrate homology of the major histocompatibility complex (MHC). Virtually all experimental work in transplantation immunology is performed using inbred strains, yet very few published studies of immune rejection in intracerebral grafts have used inbred animals.

scholarly journals The major histocompatibility complex-restricted response of recombinant inbred strains of mice to natural tick transmission of Borrelia burgdorferi.

1993 ◽  
Vol 177 (1) ◽  
pp. 9-17 ◽  
Author(s):  
W T Golde ◽  
T R Burkot ◽  
S Sviat ◽  
M G Keen ◽  
L W Mayer ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Borrelia Burgdorferi ◽  
Antibody Response ◽  
Recombinant Inbred ◽  
Inbred Strains ◽  
Recombinant Inbred Strains ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Inbred Strains Of Mice ◽  
Bacterial Antigens

The causative agent of Lyme disease, Borrelia burgdorferi, is transmitted by ticks of the Ixodes ricinus complex. In this study, we report the antibody response of recombinant inbred strains of mice of the H-2, b, d, and k haplotypes, infected with B. burgdorferi as a result of exposure to infected I. dammini. The patterns of antibody response assayed by Western blot analysis indicate significant major histocompatibility complex (MHC) restriction to bacterial antigens within the first 2 mo of infection in mice. Other bacterial antigens induce a significant response across the MHC haplotypes tested when assayed on the same bacterial strain used to transmit the infection, but do not crossreact with the same proteins derived from heterologous strains of B. burgdorferi. No response to outer surface protein A was detected at any time during the 60-d period we analyzed this infection. A third group of bacterial antigens appear to generate a MHC-nonrestricted response, and this lack of restriction is maintained when assaying the crossreactivity of the response with other strains of B. burgdorferi. These proteins may provide more accurate diagnostic probes than those currently in use. Finally, there appears to be a significant difference in the expression of most bacterial antigens when the spirochete is cultured for many passages since the same strain of bacterium isolated from low-passage and high-passage preparations exhibit different banding patterns in Western blots when assayed with the same sera.

GLUCOCORTICOID-INDUCED CLEFT PALATE IN THE MOUSE: TWO MAJOR HISTOCOMPATIBILITY COMPLEX, H-2, LOCI WITH DIFFERENT MECHANISMS

Genetics ◽  
1983 ◽  
Vol 103 (2) ◽  
pp. 263-276
Author(s):  
Joseph J Bonner ◽  
Marvin L Tyan
Keyword(s):  
Major Histocompatibility Complex ◽  
Cleft Palate ◽  
Inbred Strains ◽  
Response Analysis ◽  
Major Histocompatibility ◽  
Factors Affecting ◽  
Histocompatibility Complex ◽  
Pregnant Mice ◽  
Isolated Cleft Palate

ABSTRACT Isolated cleft palate is induced in the progeny of pregnant mice that are given glucocorticoids. The incidence varies among inbred strains and with dose and stage of gestation when the drug is given. One chromosomal region responsible for strain-associated differences in sensitivity is the major histocompatibility complex, H-2. H-2a is associated with susceptibility, H-2b with resistance. There appear to be both maternal and embryonic genetic factors affecting the sensitivity to glucocorticoids. In experiments reported here congenic strains of mice with H-2a, H-2d and H-2k haplotypes on a C57BL/10 genomic background were used. This allowed the determination of the effect on sensitivity by two H-2 subregions; the subregions are H-2K to I-E and I-C to H-2D. Methods included dose-response analysis and reciprocal cross analysis using dexamethasone given on day 12 of pregnancy. Results show that each subregion affects the strain's sensitivity to dexamethasone-induced cleft palate. The regression coefficients for B10.A-H-2a (45.4 ± 4.13) were different from those for B10.BR-H-2k (67.2 ± 10.8) and B10.D2-H-2d (70.5 ± 9.74). The estimated mean arcsine% cleft palate at 160 mg/kg was different for each strain: B10.A-H-2a, 53.1 ± 2.19; B10.BR-H-2k, 33.1 ± 2.27; B10.D2-H-2d, 25.0 ± 2.75. Different patterns of change in sensitivity were observed among the reciprocal crosses. In summary, the H-2K to I-E subregion seemed to influence both maternal and embryonic factors, whereas only embryonic factors were influenced by the I-C to H-2D subregion. These data suggest that the mechanisms affecting glucocorticoid sensitivity which are genetically encoded within each H-2 subregion are different, and there is an interaction between the alleles. The mode of interaction can be either complementation or epistasis.

scholarly journals The Resistance of BALB/cJ Mice to Yersinia pestis Maps to the Major Histocompatibility Complex of Chromosome 17

2008 ◽  
Vol 76 (9) ◽  
pp. 4092-4099 ◽  
Author(s):  
Joshua K. Turner ◽  
Milton M. McAllister ◽  
John L. Xu ◽  
Richard I. Tapping
Keyword(s):  
Major Histocompatibility Complex ◽  
Yersinia Pestis ◽  
Genetic Locus ◽  
Inbred Strains ◽  
Chromosome 17 ◽  
Surrounding Tissue ◽  
Resistance Locus ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Trait Locus

ABSTRACT Yersinia pestis, the causative agent of plague, has been well studied at the molecular and genetic levels, but little is known about the role that host genes play in combating this highly lethal pathogen. We challenged several inbred strains of mice with Y. pestis and found that BALB/cJ mice are highly resistant compared to susceptible strains such as C57BL/6J. This resistance was observed only in BALB/cJ mice and not in other BALB/c substrains. Compared to C57BL/6J mice, the BALB/cJ strain exhibited reduced bacterial burden in the spleen and liver early after infection as well as lower levels of serum interleukin-6. These differences were evident 24 h postinfection and became more pronounced with time. Although a significant influx of neutrophils in the spleen and liver was exhibited in both strains, occlusive fibrinous thrombi resulting in necrosis of the surrounding tissue was observed only in C57BL/6J mice. In an effort to identify the gene(s) responsible for resistance, we measured total splenic bacteria in 95 F2 mice 48 h postinfection and performed quantitative trait locus mapping using 58 microsatellite markers spaced throughout the genome. This analysis revealed a single nonrecessive plague resistance locus, designated prl1 (plague resistance locus 1), which coincides with the major histocompatibility complex of chromosome 17. A second screen of 95 backcrossed mice verified that this locus confers resistance to Y. pestis early in infection. Finally, eighth generation backcrossed mice harboring prl1 were found to maintain resistance in the susceptible C57BL/6J background. These results identify a novel genetic locus in BALB/cJ mice that confers resistance to Y. pestis.

scholarly journals Induction of humoral immune tolerance to major histocompatibility complex antigens by transfusions of UVB-irradiated leukocytes

Blood ◽  
1996 ◽  
Vol 88 (11) ◽  
pp. 4375-4382 ◽  
Author(s):  
KJ Kao
Keyword(s):  
Major Histocompatibility Complex ◽  
Immune Tolerance ◽  
Tolerance Induction ◽  
Inbred Strains ◽  
Mononuclear Leukocytes ◽  
Major Histocompatibility ◽  
Peripheral Blood Mononuclear ◽  
Mhc Antigens ◽  
Humoral Immune ◽  
Histocompatibility Complex

To determine whether immune tolerance to donor major histocompatibility complex (MHC) antigens can be induced by transfusions of UVB-irradiated leukocytes, studies were conducted in inbred strains of mice with well-characterized MHC antigens. CBA mice with H-2k phenotype and BALB/c mice with H-2d phenotype were used as recipients and donors, respectively. Humoral immune tolerance is defined as absence of antibody response after challenge with transfusions of untreated donor leukocytes. It was found that transfusions of purified peripheral blood mononuclear leukocytes irradiated with 1,200 mJ/cm2 UVB not only prevented allo-immunization but also induced humoral immune tolerance to donor class-I and -II MHC antigens in all recipient mice. Donor plasma and platelets interfered with the induction of this tolerance. The tolerance induction by UVB-irradiated leukocytes is dose-dependent. Four weekly transfusions of 2 x 10(5) leukocytes were required to ensure tolerance induction in all mice. The results of a long-term follow-up study showed that the induced tolerance is long-lasting and can withstand repeated challenges by untreated donor leukocytes. Recipient mice tolerant to H-2d antigens also became tolerant to H-2b, H-2r, and H-2n MHC antigens but did not have impaired antibody responses to antigens unrelated to donor leukocytes. Adoptive transfer experiments showed the development of negative regulatory cells in spleens of the tolerized mice. In view of recent feasibility of using UVB-irradiated human platelet concentrates for prevention of HLA alloimmunization, the findings of this study support that UVB- irradiated donor leukocytes could have potential, important clinical application in transplantation medicine.

scholarly journals Induction of humoral immune tolerance to major histocompatibility complex antigens by transfusions of UVB-irradiated leukocytes

Blood ◽  
1996 ◽  
Vol 88 (11) ◽  
pp. 4375-4382 ◽  
Author(s):  
KJ Kao
Keyword(s):  
Major Histocompatibility Complex ◽  
Immune Tolerance ◽  
Tolerance Induction ◽  
Inbred Strains ◽  
Mononuclear Leukocytes ◽  
Major Histocompatibility ◽  
Peripheral Blood Mononuclear ◽  
Mhc Antigens ◽  
Humoral Immune ◽  
Histocompatibility Complex

Abstract To determine whether immune tolerance to donor major histocompatibility complex (MHC) antigens can be induced by transfusions of UVB-irradiated leukocytes, studies were conducted in inbred strains of mice with well-characterized MHC antigens. CBA mice with H-2k phenotype and BALB/c mice with H-2d phenotype were used as recipients and donors, respectively. Humoral immune tolerance is defined as absence of antibody response after challenge with transfusions of untreated donor leukocytes. It was found that transfusions of purified peripheral blood mononuclear leukocytes irradiated with 1,200 mJ/cm2 UVB not only prevented allo-immunization but also induced humoral immune tolerance to donor class-I and -II MHC antigens in all recipient mice. Donor plasma and platelets interfered with the induction of this tolerance. The tolerance induction by UVB-irradiated leukocytes is dose-dependent. Four weekly transfusions of 2 x 10(5) leukocytes were required to ensure tolerance induction in all mice. The results of a long-term follow-up study showed that the induced tolerance is long-lasting and can withstand repeated challenges by untreated donor leukocytes. Recipient mice tolerant to H-2d antigens also became tolerant to H-2b, H-2r, and H-2n MHC antigens but did not have impaired antibody responses to antigens unrelated to donor leukocytes. Adoptive transfer experiments showed the development of negative regulatory cells in spleens of the tolerized mice. In view of recent feasibility of using UVB-irradiated human platelet concentrates for prevention of HLA alloimmunization, the findings of this study support that UVB- irradiated donor leukocytes could have potential, important clinical application in transplantation medicine.

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