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1.
Rev Invest Clin ; 49(3): 183-7, 1997.
Article in Spanish | MEDLINE | ID: mdl-9380972

ABSTRACT

AIM: To study the HLA markers in Mexican couples who have suffered three or more spontaneous abortions. DESIGN: The study included 24 couples with recurrent abortions and 32 with normal fertility. METHOD: HLA class I (A, B, C) and class II (DR, DQ) typing was done with a standard microlymphocytoxity test. The intergroup differences were evaluated by chi-square and the Fisher exact test. RESULTS: The frequency of the MHC markers in the males and females of couples with abortions were not significantly different from those in fertile couples. However, the abortion couples shared class I antigens more often than expected from random mating as compared to fertile couples, specially in the HLA-B locus. We also found a significantly decreased frequency of the HLA-B7 antigen in males belonging to the abortion group. CONCLUSION: These results suggest that HLA-B antigens may be markers for genes related to pregnancy outcome in Mexicans.


Subject(s)
Abortion, Habitual/immunology , HLA Antigens/analysis , Abortion, Habitual/epidemiology , Abortion, Habitual/genetics , Adult , Disease Susceptibility , Female , Fertility/genetics , Fertility/immunology , Gene Frequency , HLA Antigens/genetics , HLA-B7 Antigen/analysis , Histocompatibility Testing , Humans , Male , Mexico/epidemiology , Pregnancy , Pregnancy Outcome
2.
J Heart Lung Transplant ; 13(1 Pt 1): 129-38, 1994.
Article in English | MEDLINE | ID: mdl-8167118

ABSTRACT

Cytomegalovirus infection, a common complication in immunosuppressed graft recipients, bears an adverse impact on graft survival. Cytomegalovirus enhances the expression of the monotypic determinants of the class I major histocompatibility complex molecule by the endothelium, possibly rendering the endothelial cells more immunogenic and prone to attack by the allogeneic lymphocytes. In the present study, we focused on the effect of cytomegalovirus on the endothelial cell expression of different class I genes, on the relation between the extent of endothelial cell infection and the class I effect, and on the time course of the class I changes induced by the cytomegalovirus infection. Cytomegalovirus infection of primary cultures of human umbilical vein endothelial cells augmented the expression of the A2, A3, and B7 class I major histocompatibility complex genes when compared with uninfected cells. beta 2 microglobulin upregulation by the infected cells paralleled the changes in specific class I expression; this effect was significant only after 7 days after infection. Double immunocytochemical staining and fluorescence-activated cell sorter analysis revealed that the class I enhancement was uniform throughout the umbilical vein endothelial cell monolayer and not restricted to the cells that expressed cytomegalovirus early or late antigens. Ultraviolet-inactivated supernatants from infected umbilical vein endothelial cell did not increase class I expression on uninfected cells. In conclusion, cytomegalovirus might affect graft survival by amplifying the changes in class I expression beyond the sites of viral replication.


Subject(s)
Cytomegalovirus Infections/genetics , Cytomegalovirus Infections/immunology , Cytomegalovirus/genetics , Cytomegalovirus/immunology , Endothelium, Vascular/immunology , Gene Amplification , Gene Expression Regulation, Viral , Histocompatibility Antigens Class I/genetics , Antibody Specificity , Antigens, Viral/analysis , Cells, Cultured , Cytomegalovirus/physiology , Cytomegalovirus/radiation effects , Cytoplasm/ultrastructure , Endothelium, Vascular/microbiology , Endothelium, Vascular/ultrastructure , Gene Expression Regulation, Viral/radiation effects , HLA-A2 Antigen/analysis , HLA-A2 Antigen/genetics , HLA-A3 Antigen/analysis , HLA-A3 Antigen/genetics , HLA-B7 Antigen/analysis , HLA-B7 Antigen/genetics , Histocompatibility Antigens Class I/analysis , Humans , Ultraviolet Rays , Up-Regulation , Virus Replication , Virus Shedding , beta 2-Microglobulin/analysis , beta 2-Microglobulin/genetics
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