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At least 1,045 records · Page 58Linked to original sources
PubMed2000

[Immunogenetic aspects in pathogenesis of acute pancreatitis].

Acute pancreatitis is characterized by essential decrease of the activity of the complement C1-C5 system components which is more marked under destructive form of the disease. The increased consumption of the components of the complement may be determined by forming immune complexes under interaction of the antibodies with structural and secretory components of the pancreas and direct proteolytic conversion under influence of trypsin. The revealed associations with HLA I antigens suggest the presence of genetic determination of the changes in the complement system. It may be also possible that components of the complement system, in particular C4 which is immune product of the HLA class III region, exert regulating influence on humoral immune reactions in acute pancreatitis.

Acute Disease↗
PubMed2000

Human leukocyte antigen class I allelic and haplotype loss in squamous cell carcinoma of the head and neck: clinical and immunogenetic consequences.

The expression of human leukocyte antigen (HLA) class I molecules on the cell surface is necessary for the presentation of peptide antigens to cytotoxic CD8+ T lymphocytes of the immune system. Down-regulation of HLA class I gene expression has been implicated in tumorigenesis, including squamous cell carcinoma of the head and neck (SCCHN). Loss of MHC class I antigens may be one mechanism by which tumor cells escape immune detection. We performed prospective immunostaining of 26 primary SCCHN tumors and samples of normal mucosa harvested several centimeters away from the primary tumor, using a large panel of antibodies directed against allele-specific as well as monomorphic determinants of HLA class I molecules. Loss of expression of HLA class I proteins in the tumor was found in 50% (13 of 26) of primary tumors and was highly correlated with HLA loss in the corresponding normal mucosa (P < 0.0001). Further analysis demonstrated that the loss of HLA class I expression in the tumor was significantly associated with regional lymph node metastases (nodal stage; P = 0.0388), and that the number of HLA class I alleles lost in the normal mucosa was associated with subsequent development of a new primary aerodigestive tract cancer (P = 0.042). A patient with two metachronous cancers available for analysis had no evidence of HLA loss in the first tumor, demonstrated allelic loss in the second cancer, and subsequently died of disease. These results suggest that the loss of expression of HLA class I alleles may have prognostic implications.

Adult↗
PubMed1975

Multiple sclerosis immunogenetics. A possible correlation with human leukocyte HL-A antigens.

To investigate the relationships of genotype to susceptibility to multiple sclerosis, 42 patients hospitalized into Multiple Sclerosis Study Center of The Milan Medical School were typed for 14 HL-A specificities: HL-A1, HL-A2 + W 28, HL-A3, HL-A10 + W 19, HL-A11, HL-A9 of the 1st Series and HL-A5, HL-A7, HL-A8, HL-A12, HL-A13 of the 2nd Series. The increased HL-A9 frequency found in a previous study has been confirmed. Moreover in the total of multiple sclerosis patients this deviation reaches a higher degree of significance (P less than 0.01) and one antigen HL-A10 + W 19 appears to be significantly decreased (P less than 0.01). No variations were found in HL-A3, HL-A7 frequencies.

Clinical Trials as Topic↗
PubMed2000

[Immunologic and immunogenetic aspects of autoimmune diseases].

The primary property of the immune system is its ability to distinguish the organism's own substances from foreign bodies, to tolerate the former and to eliminate the latter. However, the immune reactions, in some cases, turn against own structures and when exceeding a particular threshold and duration, they begin to damage the tissues and organs causing autoimmune diseases.

Autoimmune Diseases↗
PubMed2000

[Immunogenetic markers in hemoblastosis].

AIM: To establish for hemoblastoses general and individual associations between HLA genes and predisposition or resistance to malignant transformation of hemopoiesis. MATERIAL AND METHODS: Antigens of class I and class II genes were determined by microlymphocytotoxic test and DNA typing (PCR-SSP) in 30 patients with acute myeloblastic leukemia (AML), 47 patients with acute lymphoblastic leukemia (ALL), 52 patients with chronic myeloblastic leukemia (CML), 58 patients with lymphogranulomatosis (LGM) and 224 donors. RESULTS: HLA specificities were elucidated frequency of which was high in all the above nosological entities: Cw7 (RR 2.5 to 5.22), DRB1*11 (RR 2.3 to 4.88). Frequency of antigen B5 was high in three diseases (RR 2.14-2.6). A number of specificities have distribution deviations typical for only one or two diseases (A19--AML and CML, B27--ALL, DRB1*08--AML). The HLA-gene was detected the frequency of which was low in three diseases--DRB1*07 (RR 0.39 to 0.11). Individual preventive HLA genes for AML, ALL, LGM were A2, B8; A1, B8, B40; DRB1*01, respectively. CONCLUSION: Cw7, DRB1*11, B5 are HLA-specificities marking hemopoiesis predisposition to malignant transformation in general. Development into a certain nosological entity depends on combination of general HLA-genes with markers of individual hemoblastosis. DRB1*07 is a general preventive gene. Preventive HLA genes can be also individual for the above hematological diseases.

Acute Disease↗
PubMed2001

Immunogenetic markers and seropositivity predict radiological progression in early rheumatoid arthritis independent of disease activity.

OBJECTIVE: A prospective clinical study of patients with recent onset rheumatoid arthritis (RA) to examine the relationship between inflammatory disease activity and joint destruction in a 4 year followup, and to evaluate prognostic markers for severe joint erosions early in the disease. METHODS: Eighty-seven patients with RA according to the American College of Rheumatology criteria and a disease duration < 2 years were followed for an observation time of 2 to 4 years (mean 3.1 yrs). Variables of clinical and laboratory disease activity were monitored, and HLA-DRB1 alleles were determined. Hand and foot radiographs were taken every 6 months. RESULTS: Multivariate analysis of independent contributions of covariates to progression of joint destruction resulted in a mixed effect regression model with significant influences for the presence of a shared epitope (SE) positive DR4 allele (SE+ DR4+; p = 0.007), rheumatoid factor (RF) IgA (p = 0.01), and sex (p = 0.059), but not for clinical variables or acute phase reactants. The odds ratio to reach a Larsen score above 32 during the observation period of 4 years was increased in patients positive for RF IgM (OR 2.7, p = 0.019), for the shared epitope on a DR4 allele (OR 8.6, p < 0.005), and in patients with erosions already at study entry (OR 11.9, p = 0.001). The highest sensitivity and specificity for the prediction of severe bone destruction (84% and 79%) were found when the presence of either a SE+ DR4 allele or of early erosions was used as a prognostic marker (OR 20.4, p < 0.0001). CONCLUSION: Our results show the pace of joint destruction in RA to be influenced by the presence of SE+ DR4 alleles, RF production, and sex and by the presence of erosive disease at presentation. Those prognostic markers exert their influence independently from the inflammatory disease activity.

Adult↗
PubMed2001

[Immunogenetic aspects of duodenal ulcer in Helicobacter pylori positive Europeans in Western Siberia].

AIM: To study HLA associations with HP-positive duodenal ulcer (DU). MATERIAL AND METHODS: A total of 47 Europeoid DU and 680 healthy subjects were examined for class I and II HLA antigens. Typing of class I antigens was conducted in the microlymphocytotoxicity test, of class 2 antigens--by polymerase chain reaction. RESULTS: The study has found associations of duodenal ulcer with HLA-A10, -B41 and different combinations of these alleles whereas HLA-A9 was protective. A relative risk of peptic ulcer was 3.03 in HLA-A10 (pcor < 0.05) and 7.78 in HLA-B41 (p < 0.001). The allele A9 occurred more frequently in healthy controls (30.15%) than in Helicobacter pylori-positive patients with DU (10.64%, RR = 3.50, pcor < 0.05). Frequencies of alleles HLA-DR7 and HLA-A1/B12 were higher in HP-positive DU patients with family history of peptic ulcer (RR = 4.00 and RR = 11.92, respectively, p < 0.05). CONCLUSION: These data suggest that HLA may influence duodenal ulcer susceptibility and resistance. The relationships help prognosticate not only development of the disease in HP infection but also the age of the infection manifestation.

Adult↗
PubMed2001

Immunogenetic factors of predisposition to duodenal ulcer in Caucasian population of western Siberia.

A total of 47 Caucasian duodenal ulcer patients and 680 healthy persons were investigated for HLA antigens of classes I and II. HLA antigens of the A, B series were sought using the microlymphocytotoxicity test, and HLA-DRBI was analysed by polymerase chain reaction. The study found associations of duodenal ulcer with HLA-A10, -B41 and different combinations of these alleles, whereas HLA-A9 was found to be protective. A relative risk of peptic ulcer was 3.03 in HLA-A10 (pcor < 0.05), and 7.78 in HLA-B41 (p < 0.001). The allele frequency A9 was higher in healthy controls (30.15%) than in Helicobacter pylori-positive patients with duodenal ulcer (10.64%, RR = 3.50, pcor < 0.05). The study showed that frequencies of alleles HLA-DR7 and HLA-A1/B12 were higher in Helicobacter pylori-positive duodenal ulcer patients with family history of peptic ulcer (RR = 4.00 and RR = 11.92, respectively p < 0.05). These data suggest that HLA may influence duodenal ulcer susceptibility and resistance, and according to the high prevalence of Helicobacter pylori (HP) infection in Siberian population (87.5%), this may occur through a non-HP infection pathway.

Adult↗
PubMed2001

[Immunogenetic cytokine restriction in multiple sclerosis].

Sixty eight patients with verified multiple sclerosis (MS) (mean EDSS score 3.1 +/- 1.0) and 50 healthy donors have been investigated. Thirty five patients had relapsing-remitting, 25--secondary progressive, 8--primary progressive course. The remission was in 38, decompensation--in 20, relapse--in 10 patients. Lymphocyte subpopulations were investigated using monoclonal antibodies (Moscow) to the following antigens: CD3 (T-lymphocytes), CD4 (T-helpers), CD8 (T-supressors), CD20 (8-lymphocytes), CD25 (IL-2 receptor), CD16 (natural killers), CD95 (activated cells ready to apoptosis). Cytokines and tumor necrosis factor-alpha (TNF-alpha) levels were measured using ELISA test. HLA antigens were investigated by standard lymphocytotoxic test. In MS we found a fall of CD3, CD4, CD8, CD20 and CD16, but an increase of CD4/CD8, CD95, CD25. The CD95 level correlated with CD4, CD4/CD8 and CD16. In MS spontaneous IL-2, IL-6, IL-8 and TNF-alpha production was raised and stimulated IL-6 and IL-8 secretion was reduced. IL-4, IL-6, IL-8, TNF-alpha and IL-1 beta serum production in vivo was elevated. We found an increase of CD3, CD4, CD16, CD25, but a decrease of IL-1 (p < 0.01) spontaneous production and IL-6, IL-8, TNF-a stimulated secretion in DR2(+) MS patients, comparing to DR2(-) patients and controls. In DR2(-) patients as compared to DR2(+) patients and controls, all lymphocyte subpopulations levels, especially CD8 (p < 0.001) one, were decreased, but spontaneous IL-8 (p < 0.01) production was increased. The data obtained indicate lymphocyte apoptosis activation, targeting promoted lymphocyte destruction, and suggest T helper type-1 reaction prevalence in MS.

Adolescent↗
PubMed2001

[Human histocompatibility HLA system. Considerations in the light of current concepts. II. Immunogenetic function].

Investigation of self-nonself recognition in the immune system has focused on classical class I and class II MHC antigens. Their extensive polymorphism and high level expression rendered them amenable to experimentation with the traditional immunologic tools, serology and transplantation. Much has been learned about their functions as a peptide--presenting receptors important for immune responses against pathogens. The central unit for regulation of the specific immune system is a trimolecular complex made up of the T cell antigen receptor (TCR), the MHC molecule and the MHC ligand. The third component is a peptide derived as a degradation product from a protein. During recent years there has been some progress in understanding the interaction between MHC molecules and their peptide ligands: MHC molecules are peptide receptors of peculiar specificity, being able to accommodate millions of different peptides provided they share some common features. In this review is to discuss the relationship between MHC molecules and their natural peptide ligands with special emphasis on MHC class I molecules, because more is known about these than class II molecules.

Genes, MHC Class I↗