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PubMed2026

Host immunogenetic variation and gut microbiome functionality in a wild vertebrate population.

BACKGROUND: The gut microbiome (GM) -important for host health and survival- is partially shaped by host immunogenetics. However, to date, no study has investigated the influence of host Major Histocompatibility Complex (MHC) genes on gut microbiome functionality in a wild population. Here we use a natural population of the Seychelles warbler (Acrocephalus sechellensis) to assess the effects of MHC genes on GM taxonomy and functionality using shotgun metagenomics. RESULTS: Our results show that taxonomic GM composition was associated with MHC-II diversity and the presence of one specific MHC-I allele (Ase-ua 7). Specifically, MHC-II diversity was associated with decreased Lactococcus lactis and increased Staphylococcus lloydii abundance, while Ase-ua 7 was linked to reduced Enterococcus casselifavus and Gordonia sp OPL2 but increased Escherichia coli and Vulcaniibacterium thermophilum. These taxonomic changes may reflect differences in MHC-mediated microbial recognition. In contrast, functional GM composition was significantly associated with increasing individual MHC-I diversity but not MHC-II diversity. In particular, increasing MHC-I diversity was associated with an increased prevalence of microbial defence genes but a reduced prevalence of microbial metabolism genes. Analysis also revealed that functional GM networks were more fragmented in high compared to low MHC-I diversity hosts. CONCLUSION: These results suggest that MHC variation (particularly at MHC-I) plays an important role in shaping both the taxonomy and function of the GM in wild vertebrates. In the Seychelles warbler, this results in trade-offs whereby there is an increase in microbial defence and a reduction in GM metabolic potential in individuals with higher MHC-I diversity. Thus, this work sheds light on the possible costs and benefits of maintaining a healthy microbiome, which is essential for understanding how the GM and immune system co-evolve. Video Abstract.

Animals↗
PubMed2003

Immunogenetic heterogeneity in single-system and multisystem langerhans cell histiocytosis.

Langerhans cell histiocytosis is a rare disease with an unknown etiology and poorly understood pathogenesis. Immunologic, viral, and proliferative clonality causes have all been considered. To determine whether Langerhans cell histiocytosis and its two main subgroups, single-system and multisystem disease, are associated with HLA-A, -B, -Cw, or -DR alleles, a total of 84 patients <15 y of age at the time of diagnosis and of Nordic origin were analyzed, 82 for HLA class I and 76 for HLA class II. Stratification of the patients into two subgroups, single-system disease (skin only, and monostotic and polyostotic disease) and multisystem disease with or without organ dysfunction, showed that patients with single-system disease (17 of 45, 38%) more often (p = 0.00018 and, after correction, p = 0.029) had the phenotype HLA-DRB1*03 compared with patients with multisystem disease (1 of 31, 3%). In the patients with multisystem disease a nonsignificant reduction of the frequency of this phenotype was seen compared with controls (p = 0.02, uncorrected). In 14 of the patients with single-system disease, but none with multisystem disease, the deduced haplotype HLA-A*01, B*08, DRB1*03 was found. High-resolution typing, performed in nine patients, revealed that all had the HLA-A*0101, B*0801, DRB1*0301, DQB1*0201 alleles. Our findings suggest an immunogenetic heterogeneity in the two clinical entities of Langerhans cell histiocytosis and indicate that HLA-DRB1*03 may play a protective role against developing multisystem disease. Further studies to confirm these findings are desired.

Adolescent↗
PubMed2005

Clinical and immunogenetic characteristics of fulminant type 1 diabetes associated with pregnancy.

OBJECTIVE: The objective of this study was to characterize the clinical and immunogenetic features of Japanese pregnancy-associated fulminant type 1 diabetes (PF). A group of patients with PF was compared with a group of patients of child-bearing age with fulminant type 1 diabetes that was not associated with pregnancy (NPF) in a nationwide survey conducted from 2000-2004. PATIENTS: The clinical characteristics of the 22 patients in the PF group were compared with those of the 48 patients in the NPF group. Human leukocyte antigen (HLA) class II DR and DQ genotyping of 17 PF and 20 NPF patients was performed. RESULTS: Arterial pH was significantly lower (P = 0.0366), and amylase values tended to increase in PF patients compared with NPF patients (P = 0.0515). In 22 PF patients, 18 developed disease during pregnancy (26.3 wk; range, 7-38), whereas four cases occurred immediately after delivery (10.5 d; range, 7-14 d). Twelve cases that developed during pregnancy resulted in stillbirth (67%), and five of the six fetal cases that survived were delivered by cesarean section. The haplotype frequency of HLA DRB1*0901-DQB1*0303 in PF was significantly higher than those in NPF (P = 0.0244) and controls (P = 0.0001), whereas that of DRB1*0405-DQB1*0401 in NPF was significantly higher than those in PF (P = 0.0162) and controls (P < 0.0001). CONCLUSIONS: The clinical symptoms of PF patients were more severe than those of NPF patients, and the prognosis of their fetuses was extremely poor. The type 1 diabetes-susceptible HLA class II haplotype is distinct in PF and NPF patients, suggesting that different HLA haplotypes underlie the presentation of PF or NPF.

Adolescent↗
PubMed1993

HLA-DQA1 and -DQB1 associations with multiple sclerosis in Sardinia and French Canada: evidence for immunogenetically distinct patient groups.

We analyzed the association of HLA-DQA1 and -DQB1 alleles with multiple sclerosis (MS) in a collaborative study of 116 Sardinian and 75 French Canadian MS patients by the relative predispositional effect method. In French Canadians, MS was positively associated with DQA1*0102 and DQB1*0602, but there was no positive association of either allele with Sardinian MS, which, by contrast, was positively associated with DQB1*0302 and *0201 and with DQA1*0301, whereas none of these alleles was MS-associated in French Canadians. In comparison with French Canadian results, DQA1*0102 was protective against MS in Sardinians. We suggest that DQA1*0102 has no MS predispositional role in French Canadians, but is MS-associated because it is in linkage disequilibrium with true predispositional alleles present within the DQB1*0602-bearing haplotype. Whereas DQB1 alleles encoding leucine (Leu) at residue 26 showed a strong MS association in French Canadians (relative risk = 24.7), there was no correlation with DQ beta Leu26 in Sardinian MS. No other DQA1 or DQB1 codons showed a positive disease correlation in both groups. Together the data suggest that the two MS patient groups are immunogenetically distinct, and it may be impossible to formulate a unifying hypothesis that explains the different MS-class II associations in these and other ethnic groups.

Alleles↗
PubMed2006

Immunocontraception of mammalian wildlife: ecological and immunogenetic issues.

Immunocontraception involves stimulating immune responses against gametes or reproductive hormones thus preventing conception. The method is being developed for the humane control of pest and overabundant populations of mammalian wildlife. This paper examines three fundamental issues associated with its use: (1) the difficulties of obtaining responses to self-antigens, (2) the likely evolution of genetically based non-response to immunocontraceptive agents, and (3) the possible changes in the array of pathogens possessed by the target species after generations of immunocontraception. Our review of the literature demonstrates that the barriers to an effective immunocontraceptive are at present very basic. Should they be overcome, the effects of immunocontraception on the immunogenetic constitution of wildlife populations through the selection for non-responders must be examined. We suggest that the attempt to use the animal's own immune system to modulate reproduction may be incompatible with the basic biological function of protection against infectious disease. Research programs on mammalian immunocontraception should involve measurement of the heritability of non-response and an assessment of the likely change in the response of the contracepted population to possible pathogens.

Animal Diseases↗
PubMed2005

[Immunogenetic factors associated with type 1 diabetes mellitus].

Type 1 diabetes mellitus has been considered an organ-specific autoimmune disease derived from the selective destruction of pancreatic beta cells. It presents a complex pathogenesis, involving the participation of several factors, including the immunogenetic susceptibility with strong association to histocompatibility genes (HLA), environmental events and autoimmune response with the presence of autoantibodies and/or autoreactive lymphocytes, culminating in metabolic abnormalities. In this study, the literature review describes mechanisms through which some factors cause susceptibility to its appearance and, additionally, prediction innovations regarding this disorder, which will certainly contribute to nursing care for patients with type 1 diabetes.

Diabetes Mellitus, Type 1↗
PubMedDate not supplied

Immunogenetical penetrance in patients with primary biliary cirrhosis.

Two family cases of primary biliary cirrhosis (PBC) followed by the existence of autoantibodies such as anti-mitochondrial antibody, anti-nuclear antibody and anti-thyroid antibody are reported. Case O M has typical PBC, however, case H E is complicated by asymptomatic polymyositis. Common haplotypes of human leukocyte antigen (HLA) were observed as A24-Bw61 in the family members of case O M who had autoantibodies. Only the mother of case H E had identical HLA haplotypes such as A2, Aw31, Bw46, Bw61, DRw8, DRw52 and DQw1. From these results, it can be suggested that immunogenetic penetrance might be associated with the occurrence of familial PBC.

Autoantibodies↗
PubMed1995

Immunogenetic, clinical, and demographic characterization of childhood type I diabetes in New Zealand.

OBJECTIVE: To examine the relationship between genetic susceptibility alleles and islet cell antibodies (ICAs) in type I diabetes. RESEARCH DESIGN AND METHODS: The human leukocyte antigen (HLA)-DQB1 alleles and ICA levels of all incident type I diabetic cases in patients < 20 years of age diagnosed in 1990 and 1991 in Canterbury, New Zealand, were determined. RESULTS: The mean annual incidence rate for type I diabetes over the 24 months was 19.0/100,000 patient-years (95% confidence interval [CI] 13.5-26.0/100,000), which was considerably higher than rates observed between 1982 and 1989 (11.7/100,000; 95% CI 9.6-14.3/100,000). ICAs > or = 10 Juvenile Diabetes Foundation units (JDF U) were present in 84.6% of the subjects, but there was a higher prevalence of ICA-negative (ICA-) subjects among those diagnosed during the winter months. The frequencies of the susceptibility allele DQB1*0302 and susceptibility genotype 0302/0201 were 71.8% and 43.5%, respectively. Subjects with 0302 tended to be younger (mean age 8.3 +/- 5.1 years) than those with nonsusceptibility types (mean age 11.8 +/- 4.7 years, P = 0.056). The probability of being ICA positive (ICA+) was not significantly different between subjects with allele 0302 (85.7%) and those without it (81.8%). All seven patients negative for ICA were homozygous for DQB1 nonaspartate-57. There was no clustering of the immunogenetic markers with demographic and clinical characteristics apart from age at diagnosis. CONCLUSIONS: No direct relationship was observed between DQB1-defined genetic susceptibility and ICA at diagnosis, suggesting that variations at the DQB1 locus are not linked to the expression of this autoimmune marker of beta-cell destruction.

Adolescent↗
PubMed1996

The low prevalence of immunogenetic markers in Korean adult-onset IDDM patients.

OBJECTIVE: IDDM is an autoimmune disease that occurs among genetically susceptible individuals. In Asian populations, it is not uncommon for adult patients with NIDDM to eventually lose beta-cell function and develop IDDM. These individuals may be characterized by autoantibodies to GAD and high-risk HLA-DQ alleles, which are unlikely to be prevalent among patients with true NIDDM or in the general population. The objective of the present study was to evaluate and compare the prevalence of these immunogenetic markers in NIDDM patients and healthy nondiabetic individuals from Korea. RESEARCH DESIGN AND METHODS: The prevalences of anti-GAD antibodies and HLA-DQA1 and DQB1 alleles among 121 patients with newly diagnosed NIDDM identified from a population-based study in Yonchon, Korea, and 100 matched healthy control subjects were evaluated and compared. RESULTS: The overall prevalence of anti-GAD antibodies was 1.7% (2 of 121) in patients with previously undiagnosed NIDDM, whereas 1 of 100 control subjects had a positive test for antibodies. Among those who tested positive, titers of antibodies to GAD were not high. No statistically significant differences in the distributions of either mean levels of anti-GAD antibodies or DQA1 and DQB1 alleles were found comparing NIDDM patients with control subjects. Interestingly, the frequency of DQB1*non-Asp-57 and DQA1*Arg-52 alleles in the Korean adult control population was similar to that in the U.S. white population (DQB1*non-Asp-57: 0.431 vs. 0.475; DQA1*Arg-52: 0.492 vs. 0.463). CONCLUSIONS: The low prevalence of anti-GAD antibodies and HLA-DQA1 and DQB1 susceptibility alleles among recent-onset NIDDM patients, which was similar to observations in control subjects, suggests that diabetes in Korean adults is unlikely to have an autoimmune component to its pathogenesis.

Adult↗
PubMed1984

Clinical significance of immunologic and immunogenetic evaluation in multiple sclerosis.

One hundred thirty-two patients were separated into clinically defined groups of definite, probable and possible multiple sclerosis (MS), the spinal cord variant of MS (SCV), and non MS neurologic disease. HLA antigens A3 and B7 occurred at increased frequencies in definite and probably MS patients when compared with neurologic controls and healthy adults. CSF elevations of either kappa/lambda ratio, IgG/total protein ratio, or IgG were seen in 65% of the definite, probable and SCV groups. Patients with HLA A3 and B7 antigens had a higher than predicted incidence of elevated kappa/lambda ratio, suggesting that there may be immunogenetic control mechanisms which influence this CSF parameter. Neither HLA antigens nor CSF protein abnormalities correlated with the age of onset, progression, or degree of disability of disease, thus limiting their prognostic usefulness.

Adolescent↗
PubMed1988

Immunogenetics of collagen-induced arthritis in rats.

CIA can be viewed as a multifactorial animal model of experimentally-induced autoimmunity that is targeted to joint tissues and under multiple gene control. Thus, although induction of CIA requires immune reactivity to type II collagen, a high immune response to type II collagen is not pathognomonic of CIA, indicating that determinant specificity is of crucial importance. Also, both RT1-linked and non-RT1-linked gene directed functions are involved in the final clinical response to immunization with type II collagen. RT1-linked control is likely exerted at the level of Class II (Ia) molecules (as it is in mice) with inherent selectivity of arthritogenic vs non-arthritogenic epitopes for presentation to the immune response system; non-RT1-linked control may reflect genes controlling T-cell receptors, immunoglobulin subtypes or complement components. There is also evidence that the effects of potentially pathological anti-collagen autoimmunity may in some strains be muted or even obviated by other non-RT1 gene controlled traits that are not directly related to the immune system. These general conclusions are in close accord with those of other investigators who have carefully conducted extensive and in-depth studies of the immunogenetics of CIA in mice. CIA is obviously not an exact model of any one of the more common rheumatic diseases, such as rheumatoid arthritis or systemic lupus erythematosus. In fact, it is more closely analogous to polychondritis and some of the other sero-negative connective tissue diseases. However, CIA remains an extremely useful model in attempts to understand the genetic and environmental factors which influence a specific and definable autoimmune process--anti-collagen reactivity. In turn, autoimmunity to collagen, and to other autoantigens, is a contributing or complicating aspect of most of the diverse human rheumatic disease syndromes which have been identified to date. The characteristics of the CIA model in rats which have been discussed in this article, i.e., genetically controlled variations in incidence, severity, rate of progression and expression of clinical disease, are also characteristic of the human rheumatic disease patient population. Likewise, the probable contribution of multiple genes to these syndromes is recognized. Continued investigation of the CIA model can be expected to yield important information that can be used to better understand its human counterparts.

Animals↗
PubMed2006

Immunogenetic phenotypes in inflammatory bowel disease.

The currently accepted etiopathogenic hypothesis suggests that the chronic intestinal inflammation and related systemic manifestations characteristic of inflammatory bowel disease (IBD) are due to an overly aggressive or pathologic immune response to resident luminal bacterial constituents. Predisposing factors are genetic dysregulation of mucosal immune responses and/or barrier function, with onset triggered by environmental stimuli. These factors and their interactions may also be important determinants of disease phenotype and disease progression. The emergence of immunogenetic phenotypes lends support to the proposed hypothesis that susceptibility genes regulate distinct immune processes, driven by luminal antigens, expressed as specific immune phenotypes which in turn influence clinical phenotypes in IBD patient.

Antibodies, Bacterial↗
PubMed1991

Immunogenetic susceptibility for post-schistosomal hepatic fibrosis.

In 19 children with hepatic fibrosis as the result of continued schistosomiasis mansoni and 20 children without hepatic fibrosis, the following studies were carried out: HLA antigen typing for 30 antigens, immune response of T lymphocytes to schistosome antigen by measuring DNA synthesis evidenced by 3H-thymidine uptake, and measurement of total OKT3+, OKT4+, and OKT8+ cells using monoclonal antibodies. Patients with hepatic fibrosis were mostly high responders in contrast with those without fibrosis. High immune response and susceptibility to post-schistosomal hepatic fibrosis were associated with a high frequency of A2 and B12 antigens and a lack of DR2 antigens, while low response was associated with the presence of the DR2 antigen. The T4+:T8+ ratio showed increased suppressor proportions in patients with low immune response and/or with no hepatic fibrosis. We suggest an immunogenetic susceptibility for post-schistosomal hepatic fibrosis, probably controlled by HLA-linked genes via the suppressor T cells.

Adolescent↗
PubMed1978

Immunogenetic determinants of familial acute lymphocytic leukemia.

Acute lymphocytic leukemia developed almost simultaneously in two adolescent brothers, and another brother and both parents had rheumatoid arthritis. Laboratory studies uncovered no evidence for an underlying immunodeficiency state in the family. Immunogenetic evaluation showed the leukemic siblings to be HLA- and mixed-leukocyte-culture identical and homozygous for a recessively inherited locus dictating the presence of antigens on the surface of B-cells. This Ia antigen, as detected by sera from mothers of leukemic children, appeared to be mapped within the major histocompatibility region and may be a human analogue to murine immune-response antigens associated with susceptibility to leukemia.

Adolescent↗
PubMed1979

Chronic Lyme arthritis. Clinical and immunogenetic differentiation from rheumatoid arthritis.

Ten patients with Lyme arthritis have developed chronic involvement of one or both knees. Lyme arthritis was diagnosed by onset with erythema chronicum migrans (six patients); residence in Lyme, Connecticut (eight); seasonal onset in summer and early fall (nine); early periods of short recurrent attacks (nine); absence of rheumatoid factor (nine); and absence of symmetrical polyarthritis, morning stiffness, subcutaneous nodules, or antinuclear antibodies (in all). Five patients had synovectomies; pannus formation and underlying cartilage erosion were present in all. Seven of the 10 patients had the same B-cell alloantigen, DRw2 (frequency in normal control subjects, 22% [P less than 0.005]), but did not have an increased frequency of the alloantigens associated with rheumatoid arthritis. Chronic Lyme arthritis, the result of an apparent tick-transmitted infection, resembles rheumatoid arthritis pathologically but generally differs from it in both prearticular and immunogenetic characteristics.

Adolescent↗
PubMed1999

Biochemical and immunogenetic analysis of an immunodominant peptide (B6dom1) encoded by the classical H7 minor histocompatibility locus.

Of the many minor histocompatibility (H) Ags that have been detected in mice, the ability to induce graft vs host disease (GVHD) after bone marrow transplantation is restricted to a limited number of immunodominant Ags. One such murine Ag, B6dom1, is presented by the H2-Db MHC class I molecule. We present biochemical evidence that the natural B6dom1 peptide is indistinguishable from AAPDNRETF, and we show that this peptide can be isolated from a wide array of tissues, with highest levels from the lymphoid organs and lung. Moreover, we employ a novel, somatic cell selection technique involving CTL-mediated immunoselection coupled with classical genetics, to show that B6dom1 is encoded by the H7 minor H locus originally discovered approximately 40 years ago. These studies provide a molecular genetic framework for understanding B6dom1, and exemplify the fact that mouse minor H loci that encode immunodominant CTL epitopes can correspond to classical H loci originally identified by their ability to confer strong resistance to tumor transplantation. Additionally, these studies demonstrate the utility of somatic cell selection approaches toward resolving H Ag immunogenetics.

Animals↗
PubMed1976

Immunogenetics and amyotrophic lateral sclerosis.

Immunological capability is to a substantial extent genetically determined. Because genetic linkage exists between histocompatibility gene loci and certain immune response gene loci, histocompatibility specificities can serve as indicators for the presence of particular inherited immunological traits. In man, certain HLA antigens seem to be associated with immunogenetic traits which result in altered susceptibility to disease with known or suspected viral or autoimmune etiologies. We have found an association between HLA-A3 and "classic" cases of ALS. The A3 antigen was present in 49% of these cases, but not in the more chronic or benign form of the disease. Five out of six "benign" cases carried HLA-B12, suggesting perhaps the presence of a trait conferring resistance to the disease. Epidemiological surveys provide evidence both for and against a correlation between the incidence of ALS and that of HLA-A3 in various population groups. Because of the multiplicity of immune response genes, susceptibility or resistance to ALS in different populations may depend on different immune response genes. The association of a disease with selected HLA antigens or phenotypes might be suggestive of a viral-allergic etiology. Evidence that bears on this hypothesis has been reviewed.

Adult↗
PubMed1978

Cross-reactivity with mouse antigens in the ferritin immunogenetic (IR-gene) system.

Structural similarity between antigens and self molecules could be responsible for low antibody responses in different immunogenetic (IR-gene) systems. B10.M and B10.D2 strains are high responders, whilst A. Thy-1-1 mice are low responders, following primary immunization with ferritin in saline. Cross-reactivity between mouse-self antigens and ferritin was tested by antigen excess and radioimmunoassay techniques, using cells obtained from normal, unimmunized high- and low-responder mice, to compete for specific antibody. Low-responder A.Thy-1-1 mouse cells consistently displaced more anti-ferritin antibodies than did high-responder B10.M and B10.D2 mouse cells at varying antibody and cell concentrations and these differences were statistically significant (P less than 0.001). It is suggested that the responder status of different strains of mice, following primary immunization with ferritin in saline, could be explained by the degree of cross-activity between self determinants and antigen, such that low responders cross-react to a greater degree with the test antigen than do high-responder mice. A similar mechanism of cross-reactivity could operate in the pathogenesis of HLA-linked diseases.

Animals↗