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1.
Tissue Antigens ; 57(4): 380-3, 2001 Apr.
Article in English | MEDLINE | ID: mdl-11380953

ABSTRACT

A new B40 allele was identified in a leukemic Caucasian patient. This allele, designated B*4013, differs in alpha 1 domain from B*4002 at six amino acidic positions: 67, 77, 80, 81, 82 and 83. Most of this substitutions could alter the antigen binding site of the HLA-B molecule. B*4013 may have originated by gene conversion or reciprocal recombination involving B*4002 as the recipient allele of sequence donated by B*4406. The new allele was serologically typed as a "blank" associated with the Bw4 epitope.


Subject(s)
Alleles , Bone Marrow Transplantation/immunology , Gene Conversion/immunology , HLA-B Antigens/genetics , Amino Acid Sequence , Base Sequence , Child , Female , HLA-B40 Antigen , Humans , Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics , Leukemia, Myelogenous, Chronic, BCR-ABL Positive/immunology , Leukemia, Myelogenous, Chronic, BCR-ABL Positive/therapy , Male , Molecular Sequence Data , Tissue Donors
2.
Nitric Oxide ; 4(5): 534-9, 2000 Oct.
Article in English | MEDLINE | ID: mdl-11020342

ABSTRACT

Much evidence supports a role of nitric oxide (.NO) and peroxynitrite (ONOO(-)) in experimental and idiopathic Parkinson's disease (PD); moreover, an overexpression of neuronal nitric oxide synthase (nNOS) was recently reported in the basal ganglia of PD patients. In accord, we previously found a 50% increased.NO production rate during the respiratory burst of circulating neutrophils (PMN) from PD patients. As PMN express the nNOS isoform, the objective of the present study was to ascertain whether this increased.NO production is representative of nNOS gene upregulation. PMN were isolated from blood samples obtained from seven PD patients and seven age- and sex-matched healthy donors; nNOS mRNA was amplified by reverse transcriptase-polymerase chain reaction and the products were hybridized with a probe for nNOS. Nitrotyrosine-containing proteins and nNOS were detected by Western blot and NO production rate was measured spectrophotometrically by the conversion of oxymyoglobin to metmyoglobin. The results showed that both.NO production and protein tyrosine nitration were significantly increased in PMN isolated from PD patients (PD 0.09 +/- 0.01 vs 0.06 +/- 0.008 nmol min(-1) 10(6) cells(-1); P < 0.05). In addition, five of the seven PD patients showed about 10-fold nNOS mRNA overexpression; while two of the seven PD patients showed an expression level similar to that of the controls; detection of nNOS protein was more evident in the former group. In summary, it is likely that overexpression of nNOS and formation of ONOO(-) in PMN cells from PD patients emphasizes a potential causal role of.NO in the physiopathology of the illness.


Subject(s)
Enzyme Induction , Neutrophils/enzymology , Nitric Oxide Synthase/genetics , Nitric Oxide Synthase/metabolism , Parkinson Disease/enzymology , Blotting, Western , Female , Humans , Hydrogen Peroxide/metabolism , Male , Middle Aged , Neutrophils/metabolism , Nitrates/metabolism , Nitric Oxide/metabolism , Nitric Oxide Synthase Type I , Parkinson Disease/genetics , Parkinson Disease/metabolism , RNA, Messenger/genetics , RNA, Messenger/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Spectrophotometry , Tyrosine/analogs & derivatives , Tyrosine/metabolism
3.
J Immunol ; 161(6): 3169-75, 1998 Sep 15.
Article in English | MEDLINE | ID: mdl-9743385

ABSTRACT

Previous studies have shown that three point mutations in exon 1 and a particular promoter haplotype of the mannan-binding lectin (MBL) gene lead to a dramatic decrease in the serum concentration of MBL. In this study, MBL genotypes and serum concentrations were determined in unrelated individuals in a population from Mozambique (n = 154) and in two native Indian tribes from Argentina (i.e., the Chiriguanos (n = 43) and the Mapuches (n = 25)). In both populations, the MBL concentrations were low compared with those found in Eskimo, Asian, and European populations. In Africans, the low serum concentrations were due to a high allele frequency (0.24) of the codon 57 (C) variant, which resulted in a high frequency of individuals with MBL deficiency (0.06), and were also due to the effect of a relatively high frequency (0.13) of low-producing promoter haplotypes. The low concentrations in the South American populations were primarily due to an extremely high allele frequency of the codon 54 (B) variant in both the Chiriguanos (0.42) and the Mapuches (0.46), resulting in high frequencies of individuals with MBL deficiency (0.14 and 0.16, respectively). In the search for additional genetic variants, we found five new promoter mutations that might help to elucidate the evolution of the MBL gene. Taken together, the results of this study show that different molecular mechanisms are the basis for low MBL levels on the two continents.


Subject(s)
Carrier Proteins/blood , Carrier Proteins/genetics , Argentina/ethnology , Base Sequence , Child , Collectins , Denmark/ethnology , Genetic Variation/immunology , Genotype , Haplotypes , Humans , Indians, South American/genetics , Lectins/blood , Lectins/genetics , Mannans/blood , Mannans/genetics , Molecular Sequence Data , Mozambique , Prospective Studies , Sequence Analysis, DNA , White People/genetics
7.
Tissue Antigens ; 46(3 ( Pt 1)): 196-203, 1995 Sep.
Article in English | MEDLINE | ID: mdl-8525479

ABSTRACT

HLA-B35, a class I antigen differentially associated to several diseases in different ethnic groups, comprises at least eight alleles which differ among them by one to six amino acids. In the present work a rapid DNA typing procedure was used to investigate the distribution of the various HLA-B35 alleles in different populations. The approach is based on a group-specific PCR amplification of a set of closely related HLA-B alleles sharing a Thr in position 45 of the alpha-1 domain. The amplified DNA was then hybridized to a panel of sequence-specific oligonucleotide (SSO) probes designed to recognize the polymorphic residues in previously reported HLA-B35 subtypes. This methodology was successfully tested in 100 individuals of four different populations, previously typed by serology as HLA-B35, and in six reference panel cells of the 10th International Histocompatibility Workshop. HLA-B*3501 was the predominant subtype in all populations. B*3502, B*3503 and, to a lesser extent B*3508, were also found. Among Mexican Mestizos, thirteen individuals had patterns of SSO hybridization suggestive of new B35 alleles. The evolutionary considerations on the different B35 alleles and their extended B35,Cw4 haplotypes are discussed.


Subject(s)
Alleles , Genes, MHC Class I , HLA-B35 Antigen/classification , HLA-B35 Antigen/genetics , Histocompatibility Testing , Base Sequence , DNA Primers , Humans , Molecular Sequence Data , Nucleic Acid Hybridization , Polymerase Chain Reaction
8.
Hepatology ; 19(6): 1371-4, 1994 Jun.
Article in English | MEDLINE | ID: mdl-8188167

ABSTRACT

We investigated the association of human leukocyte antigen antigens and type 1 chronic active "autoimmune" hepatitis in a population of 65 white Argentinian patients, taking into account the different manifestations of the disease. Standard microlymphocytotoxicity was used for human leukocyte antigen A, B, C, DR and DQ typing. Human leukocyte antigen class 2 alleles were also typed on genomic DNA by means of polymerase chain reaction amplification and hybridization to sequence specific oligonucleotides. A primary association with human leukocyte antigen DR4 was present (human leukocyte antigen DR4: 44% in patients vs. 29% in controls; chi 2, 5.6; p = 0.02, relative risk, 2.1). However, a novel association was observed with human leukocyte antigen A11 (31% in patients vs. 6% in the controls; chi 2, 25.3; corrected p = 0.001; relative risk, 6.8). Moreover, of the 20 human leukocyte antigen A11 patients, 18 had extrahepatic manifestations associated with autoimmune chronic active hepatitis. This represented 60% of the patients bearing this form of the disease (n = 30), conferring a relative risk of 22.2 (chi 2, 46.3; corrected p = 0.00008). In this group, human leukocyte antigen DR3 and DR4 had a weak association. When present together, human leukocyte antigen DR4 and human leukocyte antigen A11 had a synergistic effect, yielding an odds ratio of 357. Statistical analysis and family segregation studies suggest that the two loci products may represent independent risk factors for this form of autoimmune chronic active hepatitis. This synergistic effect was not evident with A11 plus DR3. In autoimmune chronic active hepatitis patients without extrahepatic manifestations, a weak association with human leukocyte antigen DR6 was found.(ABSTRACT TRUNCATED AT 250 WORDS)


Subject(s)
Autoimmune Diseases/immunology , HLA Antigens/blood , Hepatitis, Chronic/immunology , Adolescent , Adult , Aged , Alleles , Argentina/epidemiology , Autoimmune Diseases/epidemiology , Autoimmune Diseases/genetics , Chi-Square Distribution , Female , Follow-Up Studies , Gene Frequency , Genetic Predisposition to Disease , HLA Antigens/classification , HLA Antigens/genetics , Hepatitis, Chronic/epidemiology , Hepatitis, Chronic/genetics , Humans , Male , Middle Aged , Odds Ratio , Risk Factors
9.
Tissue Antigens ; 43(2): 83-7, 1994 Feb.
Article in English | MEDLINE | ID: mdl-8016846

ABSTRACT

In the present study, the polymorphic domain of HLA class II genes present in a pediatric population of Argentinian celiac disease patients was analyzed by hybridization to sequence-specific oligonucleotides and DNA sequencing. Sixteen out of 16 DR5/7 heterozygous patients bore the DQA1*0501 and DQB1*0201 alleles implicated in the DQ2 risk specificity. The second exon of DQA1, DQB1 and DRB1 genes from 2 DR5/7 patients was characterized by DNA sequencing. The following alleles were found in both patients: DRB1*1101 and DRB1*0701; DQB1*0301 and DQB1*0201; DQA1*0501 and DQA1*0201. Previous serological analysis in this population had shown the presence of DQ2 in 95% of the patients (40% in controls) and a negative association with DQ1 haplotypes, suggesting the presence of other "permissive" or neutral alleles. The following HLA-DQB1 alleles, besides DQB1*0201, were identified in 31 CD patients: DQB1*0301, 0302, 0401 and 0402. All these alleles share a common pattern of residues between positions 84 and 90, and distinct from that present in DQ1-related alleles.


Subject(s)
Celiac Disease/genetics , Celiac Disease/immunology , Histocompatibility Antigens Class II/genetics , White People/genetics , Alleles , Amino Acid Sequence , Argentina/ethnology , Celiac Disease/ethnology , Child , DNA/analysis , DNA/genetics , Exons , HLA-DQ Antigens/genetics , HLA-DR5 Antigen/genetics , Heterozygote , Humans , Molecular Sequence Data
11.
Tissue Antigens ; 41(3): 143-7, 1993 Mar.
Article in English | MEDLINE | ID: mdl-8316945

ABSTRACT

Human minor histocompatibility antigen-specific, HLA-B*3501-restricted cytotoxic T-cell clones were assayed on a panel of 25 different target cells previously typed by serology as HLA-B35. Cells from 6 donors were not killed and cells from 2 of these were further studied by molecular cloning to characterize their HLA class I alleles. Two new HLA-B35 subtypes were identified. The sequence of one of them differs from B*3501 by one nucleotide change at codon 156, replacing a Leu for an Arg. The sequence of the other new subtype also shows a single nucleotide change compared to B*3501, with Gly-->Val substitution at residue 16. With these new variants, the allelic complexity of HLA-B35 extends now to eight subtypes.


Subject(s)
Alleles , Genes, MHC Class I , HLA-B35 Antigen/classification , Amino Acid Sequence , Base Sequence , Consensus Sequence , Cytotoxicity Tests, Immunologic , DNA/genetics , HLA-B35 Antigen/genetics , HLA-B35 Antigen/immunology , Humans , Models, Molecular , Molecular Sequence Data , Protein Conformation , Recombinant Proteins/genetics , Recombinant Proteins/immunology , Sequence Alignment , Sequence Homology
12.
Hum Immunol ; 31(3): 153-8, 1991 Jul.
Article in English | MEDLINE | ID: mdl-1890016

ABSTRACT

The primary structure of an HLA class I genomic clone isolated from a homozygous HLA-B35 Caucasian individual of hispanic origin was determined. The nucleotide sequence of exons 1, 2, 4, 5, 6, and 7 is identical to that of the HLA-B35 allele of Oriental origin reported previously. Exon 3 differs in only three nucleotides present in a stretch of 23 bp. These changes introduce three amino acid substitutions in residues 109 (Leu----Phe), 114 (Asp----Asn), and 116 (Ser----Tyr), two of which (114 and 116) are located in one of the beta sheets at the bottom of the peptide binding site. The nature of these replacements in this HLA-B35 variant is likely to affect peptide binding and recognition by T lymphocytes. Introns 1, 2, 3, 4, 5, and 6 from this genomic clone are identical to those present in HLA-Bw58, further confirming the evolutionary origin of HLA-B35.


Subject(s)
Genes, MHC Class I , HLA-B35 Antigen/genetics , Amino Acid Sequence , Argentina , Base Sequence , Female , Genetic Variation , Humans , Introns , Molecular Sequence Data , Sequence Homology, Nucleic Acid , Spain/ethnology , White People/genetics
13.
Medicina (B Aires) ; 51(2): 151-4, 1991.
Article in Spanish | MEDLINE | ID: mdl-1820502

ABSTRACT

A 20-year old patient is presented with generalized lymphadenopathy, splenomegaly, hyperleukocytosis and a bone marrow biopsy showing panmyelosis with predominance of immature granulocytes. Lymph node biopsy showed a histopathological feature that was diagnosed as a chronic granulocytic leukemia in blast crisis. The cell surface phenotype of these blast cells showed predominance of immature CD1+, CD7+ T lymphocytes. The T cell lineage was confirmed by DNA rearrangement studies. In addition, the patient showed erythrocytosis, arterial O2 saturation of 92% and thrombocytosis, characteristics of polycythemia vera. After chemotherapy, the patient relapsed with similar symptoms and lymph node cells of similar immature T phenotype. With a revised diagnosis of immature T cell lymphoma associated to a myeloproliferative disorder and polyglobulia, the patient received a combined treatment of Cyclophosphamide-Adriamycin-Vincristine-VM26-Prednisone. Two months later, the patient relapsed again. He received the first phase of induction of the BFM protocol, with partial clinical remission. Five months later, the patient returned with fever, polyadenopathy and splenomegaly. Lymph node cells showed again immature T cell phenotype. The patient was next treated with the m-BACOD scheme, with no response and progression of the disease and he died few days later due to massive bleeding and cardiorespiratory failure.


Subject(s)
Lymph Nodes/pathology , Lymphoma, T-Cell/complications , Polycythemia Vera/complications , Adult , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Biopsy , Blast Crisis , Gene Rearrangement , Humans , Lymphoma, T-Cell/drug therapy , Lymphoma, T-Cell/pathology , Male , Polycythemia Vera/diagnosis
14.
Medicina (B.Aires) ; 51(2): 151-4, 1991. ilus
Article in Spanish | LILACS | ID: lil-105422

ABSTRACT

Se presenta un paciente de 20 años con poliadenopatías, esplenomegalia hiperleucocitosis y una biopsia de médula ósea que mostró una panmielosis con predominio d eelementos inmaduros. El estudio histopatológico de la biopsia de un ganglio linfático sugirió el diagnóstico de leucemia mieloide crónica en crisis blástica. El fenotipo inmunológico de las células blásticas mostró predominio de celulas T con fenotipo inmaduro CS1+, CD7+. El linaje celular T se confirmó por estudios de reordenamiento genético. Presenta además eritrocitosis, saturación arterial de O2 de 92% y trombocitosis, características de policitemia vera. Luego de quimioterapia Vincristina y Prednisona, recae a los dos meses con síntomas similares y con células de ganglio linfático del mismo fenotipo T inmaduro. Se replantea el diagnóstico como linfoma T asociado a un síndrome mieloproliferativo y policitemia, y se lo trata con Ciclofosfamida-Vincristina-VM26-Prednisona. Luego de una segunda recaída, dos meses después, se le indica un protocolo BFM, al que responde parcialmente. Cinco meses después el paciente presenta una tercera recaída, donde las células de ganglio muestran nuevamente fenotipo T inmaduro. No responde a un tratamiento con esquema m-BACOD, la enfermedad progresa, falleciendo luego de una hemorragia masiva por un paro cardiorespiratorio


Subject(s)
Adult , Humans , Male , Lymph Nodes/pathology , Lymphoma, T-Cell/complications , Polycythemia Vera/complications , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Blast Crisis , Gene Rearrangement , Lymphoma, T-Cell/drug therapy , Lymphoma, T-Cell/pathology , Polycythemia Vera/diagnosis
15.
Medicina [B Aires] ; 51(2): 151-4, 1991.
Article in Spanish | BINACIS | ID: bin-51331

ABSTRACT

A 20-year old patient is presented with generalized lymphadenopathy, splenomegaly, hyperleukocytosis and a bone marrow biopsy showing panmyelosis with predominance of immature granulocytes. Lymph node biopsy showed a histopathological feature that was diagnosed as a chronic granulocytic leukemia in blast crisis. The cell surface phenotype of these blast cells showed predominance of immature CD1+, CD7+ T lymphocytes. The T cell lineage was confirmed by DNA rearrangement studies. In addition, the patient showed erythrocytosis, arterial O2 saturation of 92


and thrombocytosis, characteristics of polycythemia vera. After chemotherapy, the patient relapsed with similar symptoms and lymph node cells of similar immature T phenotype. With a revised diagnosis of immature T cell lymphoma associated to a myeloproliferative disorder and polyglobulia, the patient received a combined treatment of Cyclophosphamide-Adriamycin-Vincristine-VM26-Prednisone. Two months later, the patient relapsed again. He received the first phase of induction of the BFM protocol, with partial clinical remission. Five months later, the patient returned with fever, polyadenopathy and splenomegaly. Lymph node cells showed again immature T cell phenotype. The patient was next treated with the m-BACOD scheme, with no response and progression of the disease and he died few days later due to massive bleeding and cardiorespiratory failure.

16.
Medicina [B.Aires] ; 51(2): 151-4, 1991. ilus
Article in Spanish | BINACIS | ID: bin-26631

ABSTRACT

Se presenta un paciente de 20 años con poliadenopatías, esplenomegalia hiperleucocitosis y una biopsia de médula ósea que mostró una panmielosis con predominio d eelementos inmaduros. El estudio histopatológico de la biopsia de un ganglio linfático sugirió el diagnóstico de leucemia mieloide crónica en crisis blástica. El fenotipo inmunológico de las células blásticas mostró predominio de celulas T con fenotipo inmaduro CS1+, CD7+. El linaje celular T se confirmó por estudios de reordenamiento genético. Presenta además eritrocitosis, saturación arterial de O2 de 92% y trombocitosis, características de policitemia vera. Luego de quimioterapia Vincristina y Prednisona, recae a los dos meses con síntomas similares y con células de ganglio linfático del mismo fenotipo T inmaduro. Se replantea el diagnóstico como linfoma T asociado a un síndrome mieloproliferativo y policitemia, y se lo trata con Ciclofosfamida-Vincristina-VM26-Prednisona. Luego de una segunda recaída, dos meses después, se le indica un protocolo BFM, al que responde parcialmente. Cinco meses después el paciente presenta una tercera recaída, donde las células de ganglio muestran nuevamente fenotipo T inmaduro. No responde a un tratamiento con esquema m-BACOD, la enfermedad progresa, falleciendo luego de una hemorragia masiva por un paro cardiorespiratorio (AU)


Subject(s)
Adult , Humans , Male , Lymphoma, T-Cell/complications , Polycythemia Vera/complications , Lymph Nodes/pathology , Lymphoma, T-Cell/pathology , Lymphoma, T-Cell/drug therapy , Polycythemia Vera/diagnosis , Blast Crisis , Gene Rearrangement , Antineoplastic Combined Chemotherapy Protocols/therapeutic use
17.
Dis Markers ; 8(5): 265-74, 1990.
Article in English | MEDLINE | ID: mdl-1707769

ABSTRACT

One hundred and ninety well-characterized acute and chronic leukaemias were studied for the expression of CD1a antigen by indirect immunofluorescence (IIF). CD1a was detected on 28 per cent of mature B cell lymphoproliferative disorders, 26 per cent of acute non-lymphoblastic leukaemias (ANLL), 21 per cent of chronic granulocytic leukaemias in blast crisis (CML-BC), 53 percent of T acute lymphocytic leukaemias (T-ALL) and in only one out of 35 common acute lymphoblastic leukaemias (c-ALL). In some cases the expression of the CD1a antigen on the surface of leukaemic cells showed a spontaneous fluctuation after a short period of incubation in vitro. CD1b and CD1c molecules were also detected on B cells and acute non-lymphoblastic leukaemias. The presence of CD1 antigens was confirmed using a dot blot assay (DBA) on the lysate of leukaemic cells.


Subject(s)
Antigens, Differentiation/analysis , Biomarkers, Tumor/analysis , Leukemia/immunology , Antigens, CD/analysis , Antigens, CD/classification , Antigens, CD1 , Antigens, Differentiation/classification , Biomarkers, Tumor/classification , Humans , Leukemia, B-Cell/immunology , Leukemia, Myeloid, Accelerated Phase/immunology , Leukemia, Myeloid, Acute/immunology , Leukemia-Lymphoma, Adult T-Cell/immunology
18.
Hum Immunol ; 26(4): 272-80, 1989 Dec.
Article in English | MEDLINE | ID: mdl-2573590

ABSTRACT

In the present study Latin-American celiac disease patients were analyzed for the frequency of certain HLA class II restriction fragment length polymorphisms in order to investigate whether they exhibited the normal associated alleles or showed unusual class II variants. A DPB/RsaI 4.0-kb fragment that was shown to be significantly increased among North Americans celiac disease patients of the DR3,DQw2 haplotype was found with similar frequency in Latin-American control and celiac disease individuals. A DPA/BglII 3.7-kb fragment previously shown to be increased among British celiac disease patients was also present with similar frequency among Latin-American control and celiac disease individuals. These results show that the frequency of the HLA-DP region-derived restriction fragment length polymorphisms linked to celiac disease differs between Caucasian populations of different ethnic backgrounds (Anglo-Saxon and Latin-American). On the other hand, DNA samples from 13 patients and 14 controls bearing the DR5/DR7 phenotype (which is significantly associated with celiac disease in Latin populations) were investigated for the presence of particular restriction fragment length polymorphisms disproportionally present in celiac disease individuals. No significant differences were found between controls and patients when the DNA was analyzed with 10 different restriction enzymes and probes for DRB, DQA, DQB, and DPB HLA class II sequences.


Subject(s)
Celiac Disease/genetics , Genes, MHC Class II , Polymorphism, Restriction Fragment Length , Alleles , Celiac Disease/immunology , Child , DNA/analysis , Female , HLA-DP Antigens/genetics , Humans , Latin America , Male , Phenotype , White People/genetics
19.
Medicina (B Aires) ; 49(2): 119-24, 1989.
Article in Spanish | MEDLINE | ID: mdl-2577009

ABSTRACT

In this report we discuss the results of the association of chronic active hepatitis (B virus) and coeliac disease with HLA class I and class II antigens, in patients of Latin American Caucasian origin. Evidence is presented showing that the alleles involved differ from those reported in other Caucasian populations of different ethnic background. Differences were observed both at the serology and at the DNA (RFLP) level. The relevance of these findings regarding the clinical implications as well as the molecular mechanisms involved in the associations are discussed.


Subject(s)
Celiac Disease/genetics , HLA Antigens/genetics , Hepatitis, Chronic/genetics , Polymorphism, Restriction Fragment Length , Argentina , Celiac Disease/ethnology , Celiac Disease/immunology , Gene Frequency , HLA-B35 Antigen/genetics , Hepatitis, Chronic/ethnology , Hepatitis, Chronic/immunology , Humans
20.
Medicina (B.Aires) ; 49(2): 119-24, 1989. tab, ilus
Article in Spanish | LILACS | ID: lil-85317

ABSTRACT

En este trabajo se describen los resultados de dos estudios de asociación de patologías a determinados alelos de clase I y clase II del sistema HLA en pacientes caucásicos argentinos: la hepatitis crónica activa (virus B) y la enfermedad celíaca. Se presentan evidencias que muestran para ambas patologías que los alelos HLA involucrados no son los mismos que los hallados para otros grupos éticos. Estas diferencias residen tanto a nivel serológico como a nivel del DNA (evaluable por RFLP). Estos hallazgos son relevantes tanto en lo referente a las aplicaciones clínicas de las asociaciones descriptas (por ejemplo la tipificación de hermanos o hijos de pacientes celíacos para identificar a los portadores de los alelos de riesgo), como así también para invetigar las bases moleculares de las maismas


Subject(s)
Humans , HLA Antigens/genetics , Celiac Disease/genetics , Hepatitis, Chronic/genetics , Polymorphism, Restriction Fragment Length , HLA Antigens/genetics , Argentina , Celiac Disease/immunology , Gene Frequency , Hepatitis, Chronic/immunology
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