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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.
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
4.
Jan Klein Christophe Benoist Chella S. David Peter Demant Kirsten Fischer Lindahl Lorraine Flaherty Richard A. Flavell Ulrich Hämmerling Leroy E. Hood Stephen W. Hunt III Patricia P. Jones Philippe Kourilsky Hugh O. McDevitt Daniel Meruelo Donal B. Murphy Stanley G. Nathenson David H. Sachs Michael Steinmetz Susumu Tonegawa Edward K. Wakeland Elizabeth H. Weiss 《Immunogenetics》1990,32(3):147-149
5.
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
6.
Ian W. Pray Francesco Pizzitutti Gabrielle Bonnet Eloy Gonzales-Gustavson Wayne Wakeland William K. Pan William E. Lambert Armando E. Gonzalez Hector H. Garcia Seth E. ONeal for the Cysticercosis Working Group in Peru. 《PLoS neglected tropical diseases》2021,15(10)
BackgroundThe pork tapeworm (Taenia solium) is a parasitic helminth that imposes a major health and economic burden on poor rural populations around the world. As recognized by the World Health Organization, a key barrier for achieving control of T. solium is the lack of an accurate and validated simulation model with which to study transmission and evaluate available control and elimination strategies. CystiAgent is a spatially-explicit agent based model for T. solium that is unique among T. solium models in its ability to represent key spatial and environmental features of transmission and simulate spatially targeted interventions, such as ring strategy.Methods/Principal findingsWe validated CystiAgent against results from the Ring Strategy Trial (RST)–a large cluster-randomized trial conducted in northern Peru that evaluated six unique interventions for T. solium control in 23 villages. For the validation, each intervention strategy was replicated in CystiAgent, and the simulated prevalences of human taeniasis, porcine cysticercosis, and porcine seroincidence were compared against prevalence estimates from the trial. Results showed that CystiAgent produced declines in transmission in response to each of the six intervention strategies, but overestimated the effect of interventions in the majority of villages; simulated prevalences for human taenasis and porcine cysticercosis at the end of the trial were a median of 0.53 and 5.0 percentages points less than prevalence observed at the end of the trial, respectively.Conclusions/SignificanceThe validation of CystiAgent represented an important step towards developing an accurate and reliable T. solium transmission model that can be deployed to fill critical gaps in our understanding of T. solium transmission and control. To improve model accuracy, future versions would benefit from improved data on pig immunity and resistance, field effectiveness of anti-helminthic treatment, and factors driving spatial clustering of T. solium infections including dispersion and contact with T. solium eggs in the environment. 相似文献
7.
8.
9.
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
10.
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