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排序方式: 共有92条查询结果,搜索用时 328 毫秒
1.
The restriction fragment length polymorphism (RFLP) of DQ
was assessed in a panel of control and insulin-dependent diabetes (IDD) patients who were serologically typed as HLA-DR4 homozygotes or HLA-DR3, DR4 heterozygotes. Digestions of genomic DNA with Barn HI, Bg1 II, Pst I, Xba I, and Hind III revealed a total of 15 RFLPs in the panel of 71 HLA-DR4 chromosomes. These RFLPs were organized into six allelic groups on the basis of segregation analysis in families. Complete RFLP haplotypes for the 5 restriction enzymes could be constructed for 42 of the HLA-DR4 chromosomes. This analysis revealed 18 RFLP haplotypes of DQ
associated with the DR4 chromosomes tested. Two of these haplotypes, designated DQ3.DR4.a and DQ3.DR4.b, accounted for over 50 % of the DR4 chromosomes analyzed. These two haplotypes were antithetical for the RFLPs detected by all five enzymes, indicating that they represent very distinct forms of DQ
. The remaining 16 haplotypes were infrequent or unique and were closely related to either a DQ3.DR4.a or DQ3.DR4.b. Two of the RFLPs detected, a 5.8 kb Bg1 II fragment and a 10.5 kb Barn HI fragment, had increased frequencies in disease-associated chromosomes. However, none of the RFLPs we detected exhibited a statistically significant increase in IDD or control populations. In contrast, the DQ3.DR4.b DQ
haplotype was significantly decreased in IDD-associated DR4 chromosomes. (P=0.04). These results suggest that the DQ3.DR4.b DQ
allele may be protective for the development of IDD. 相似文献
2.
Variant class II molecules from H-2 haplotypes in wild mouse populations: functional characteristics of closely related class II gene products 总被引:1,自引:0,他引:1
Independently derived haplotypes found in wild populations of mice often express class II molecules antigenically related to specific alleles of the A molecules defined in laboratory mice. Tryptic peptide fingerprint comparisons of these antigenically related molecules indicate that they have similar, or possibly identical, primary structures in the A alpha, A beta, or both subunits. By using the Ak and Ap families of independently derived, antigenically related A molecules, we examined the effect that minor structural variations in the A molecule have on allorecognition by T lymphocytes. Data obtained indicate that a) minor structural variations in the A molecule can effect, although not always, major functional changes in allorecognition, b) changes in allorecognition are always detected when the A beta subunit contains structural variations, but not necessarily when the A alpha subunit contains structural variations, and c) more than one site in the A molecule can be recognized by alloreactive T lymphocytes. These results can be interpreted as indicating that specific sites within the A molecule are critically involved in allorecognition and that structural variations must affect these sites to elicit major changes in allorecognition. 相似文献
3.
Recent evidence from both population data and DNA sequence analyses indicates that the unprecedented genetic diversity found at MHC loci is selectively maintained in contemporary natural populations, although the strength and nature of this selection are currently unclear. Due to the critical role played by MHC molecules in immune recognition, it is generally assumed that some form of parasite-driven selection is operating. However, the general failure to implicate MHC in the susceptibility to specific infectious diseases has been troubling, and may indicate that selection is too weak to detect directly. Alternatively, strong selection can be reconciled by a variety of factors including the amplification of minor (disease-based) vigor differences into large fitness differences by intraspecific competition, or non-disease-based selection such as mating preferences and selective abortion. 相似文献
4.
Production of congenic mouse strains carrying genomic intervals containing SLE-susceptibility genes derived from the SLE-prone NZM2410 strain 总被引:12,自引:0,他引:12
Systemic lupus erythematosus is inherited as a complex polygenic trait. Four genomic intervals containing major SLE-susceptibility
loci were previously identified by interval mapping in the NZM2410 mouse model. In this paper, we utilized a marker-assisted
selection protocol to produce four congenic mouse strains, each carrying an NZM2410-derived SLE-susceptibility interval on
a C57BL/6-resistant background. Each strain carries only one susceptibility allele derived from this polygenic model and consequently
can be used to characterize the specific component phenotypes contributed by individual SLE-susceptibility genes. We illustrate
the efficacy of this approach with phenotypic data for one of our congenic strains, B6.NZMH2
z
. Our results indicate that this single genomic interval from Chromosome (Chr) 17 of NZM2410 can mediate increased levels of
IgG autoantibodies specific for chromatin and that, similar to results obtained in our original genetic cross, B6.NZMH2
z/b
heterozygotes are more prone than B6.NZMH2
z
homozygotes to the development of humoral autoimmunity to nuclear antigens. These results illustrate the feasibility of using
congenic strains to dissect the complex pathogenic mechanisms that mediate polygenic SLE. These congenic strains will be valuable
tools in the genetic analysis of SLE susceptibility. In future studies, these congenic strains will be interbred to produce
bi- and tri-congenic strains in order to assess the role of genetic interactions in the expression of specific components
of SLE pathogenesis. They will also be instrumental to the positional cloning and identification of the genes responsible
for SLE susceptibility, via the production of congenic recombinants.
Received: 1 September 1995 / Accepted: 20 December 1995 相似文献
5.
Sujay K. Singh Edward K. Wakeland Ivica Vučak Zoltan A. Nagy Jan Klein 《Immunogenetics》1981,14(3-4):273-281
The B10.STA62 strain carries the H-2
w27 haplotype derived from a wild mouse captured in the vicinity of Ann Arbor, Michigan. Products of two class II loci composing this haplotype, A
and A
, are serologically, biochemically (by tryptic peptide mapping), and functionally indistinguishable from products controlled by the A
b
and A
/b
genes of the B10.A(5R) strain. In contrast, the polypeptide chain controlled by the third class II locus, E
, is different from that controlled by the E
/b
gene. This E
/w27
chain lacks an antigenic determinant present on the Eb molecule and carries determinants lacking on the Eb molecule, the E
/b
and E
/w27
peptide maps differ in at least six peptides, and cytotoxic T cells specific for the E
b
chains do not react with B10.STA62 target cells. This great difference between the E
/b
and E
/w27
chains suggests that the corresponding genes have not been derived from one another by a direct mutational conversion; instead, H-2
w27 appears to be a recombinant haplotype derived by crossing-over between the A
A
duplex and the E
locus. This is the first recombinant discovered separating these class II loci. 相似文献
6.
7.
8.
Subramanian S Yim YS Liu K Tus K Zhou XJ Wakeland EK 《Journal of immunology (Baltimore, Md. : 1950)》2005,175(2):1062-1072
Sle is a susceptibility locus for systemic autoimmunity derived from the lupus-prone NZM2410 mouse. The New Zealand White-derived suppressive modifier Sles1 was identified as a specific modifier of Sle1 and prevents the development of IgG anti-chromatin autoantibodies mediated by Sle1 on the C57BL/6 (B6) background. Fine mapping of Sles1 with truncated congenic intervals localizes it to a approximately 956-kb segment of mouse chromosome 17. Sles1 completely abrogates the development of activated T and B cell populations in B6.Sle1. Despite this suppression of the Sle1-mediated cell surface activation phenotypes, B6.Sle1 Sles1 splenic B cells still exhibit intrinsic ERK phosphorylation. Classic genetic complementation tests using the nonautoimmmune 129/SvJ mouse suggests that this strain possesses a Sles1 allele complementary to that of New Zealand White, as evidenced by the lack of glomerulonephritis, splenomegaly, and antinuclear autoantibody production seen in (129 x B6.Sle1 Sles1)F(1)s. These findings localize and characterize the suppressive properties of Sles1 and implicate 129 as a useful strain for aiding in the identification of this elusive epistatic modifier gene. 相似文献
9.
Lessard CJ Adrianto I Ice JA Wiley GB Kelly JA Glenn SB Adler AJ Li H Rasmussen A Williams AH Ziegler J Comeau ME Marion M Wakeland BE Liang C Ramos PS Grundahl KM Gallant CJ Alarcón-Riquelme ME Alarcón GS Anaya JM Bae SC Boackle SA Brown EE Chang DM Cho SK Criswell LA Edberg JC Freedman BI Gilkeson GS Jacob CO James JA Kamen DL Kimberly RP Kim JH Martin J Merrill JT Niewold TB Park SY Petri MA Pons-Estel BA Ramsey-Goldman R Reveille JD Scofield RH Song YW Stevens AM Tsao BP Vila LM Vyse TJ 《American journal of human genetics》2012,90(4):648-660
Systemic lupus erythematosus (SLE) is a chronic heterogeneous autoimmune disorder characterized by the loss of tolerance to self-antigens and dysregulated interferon responses. The etiology of SLE is complex, involving both heritable and environmental factors. Candidate-gene studies and genome-wide association (GWA) scans have been successful in identifying new loci that contribute to disease susceptibility; however, much of the heritable risk has yet to be identified. In this study, we sought to replicate 1,580 variants showing suggestive association with SLE in a previously published GWA scan of European Americans; we tested a multiethnic population consisting of 7,998 SLE cases and 7,492 controls of European, African American, Asian, Hispanic, Gullah, and Amerindian ancestry to find association with the disease. Several genes relevant to immunological pathways showed association with SLE. Three loci exceeded the genome-wide significance threshold: interferon regulatory factor 8 (IRF8; rs11644034; pmeta-Euro = 2.08 × 10−10), transmembrane protein 39A (TMEM39A; rs1132200; pmeta-all = 8.62 × 10−9), and 17q21 (rs1453560; pmeta-all = 3.48 × 10−10) between IKAROS family of zinc finger 3 (AIOLOS; IKZF3) and zona pellucida binding protein 2 (ZPBP2). Fine mapping, resequencing, imputation, and haplotype analysis of IRF8 indicated that three independent effects tagged by rs8046526, rs450443, and rs4843869, respectively, were required for risk in individuals of European ancestry. Eleven additional replicated effects (5 × 10−8 < pmeta-Euro < 9.99 × 10−5) were observed with CFHR1, CADM2, LOC730109/IL12A, LPP, LOC63920, SLU7, ADAMTSL1, C10orf64, OR8D4, FAM19A2, and STXBP6. The results of this study increase the number of confirmed SLE risk loci and identify others warranting further investigation. 相似文献
10.
Ophioglossum petiolatum . Unlike Angiopteris (Marattiales), which is monoplastidic, Ophioglossum undergoes polyplastidic meiosis like members of the fern-seed plant clade. The meiotic spindle is distinctly multipolar in
origin and is consolidated into a bipolar spindle that is variously twisted and curved to accommodate the large number of
chromosomes. Although a phragmoplast forms after first meiosis, no wall is deposited. Instead, an organelle band consisting
of intermingled plastids and mitochondria is formed in the equatorial region between the dyad domains. Following second meiosis,
a complex of phragmoplasts forms among sister and non-sister nuclei. Cell plates are deposited first between sister nuclei
and then in the region of the organelle band resulting in a tetrad of spores each with a equal allotment of organelles.
Received 30 January 2001/ Accepted in revised form 24 April 2001 相似文献