PubMed Health⌕ Search

Biomedical subjects

G Kreeb

Publications and source records attributed to G Kreeb.

15 recordsLinked to original sources
PubMed1985

Changing biclonal gammopathy due to different lymphocyte clones in acquired immunodeficiency syndrome with Kaposi's sarcoma.

We report the first case of acquired immunodeficiency-syndrome (AIDS) with Kaposi's sarcoma which at the same time has also a changing biclonal gammopathy (initial: double IgG-paraproteinaemia, later on IgA-IgG double-paraproteinaemia) due to different lymphocyte clones. The relationship of a B-cell neoplasia to a concurrent disease of T-cells is discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1985

IgG-antibodies to HTLV-III in patients with AIDS, LAS, and persons at risk of AIDS in West Germany.

In a first seroepidemiological study on the prevalence of the human T-lymphotropic retrovirus HTLV-III in West Germany, sera of 26 patients with acquired immunodeficiency syndrome (AIDS), 33 patients with lymphadenopathy syndrome (LAS) or AIDS related complex (ARC), and 113 homosexual men at risk of AIDS were screened for IgG antibodies to HTLV-III by an enzyme linked immunosorbent assay (ELISA). 22 out of 26 AIDS-patients (84.6%), 24 out of 33 LAS-patients (72.7%), and 44 out of 113 healthy homosexual men with increased risk of AIDS (38.9%) were found positive for antibodies to HTLV-III. Heterosexual controls including healthy laboratory workers and medical personnel with contact to AIDS patients did not show antibodies to HTLV-III. The HTLV-III antibodies analyzed predominantly recognize a protein of molecular weight 41,000 (p41).

Acquired Immunodeficiency Syndrome↗
PubMed1985

Antigens and circulating immune complexes related to the primate retroviral glycoprotein SiSV gp70: prevalence and distribution in human sera.

We have shown previously that antigens and also circulating immune complexes related to the primate retroviral envelope glycoprotein SiSV gp70 correlate with early mortality and survival of 56 patients with acute leukemias and chronic myelogenous leukemia in blast crisis. The prevalence and general distribution of these antigens and immune complexes in human sera was therefore of obvious interest. We now report an analysis of a total of 200 sera from 166 patients. Of these 113 sera were obtained from 84 patients with acute or chronic leukemias and 87 from 82 non-leukemic subjects, including laboratory workers and patients with non-leukemic neoplasias. Antigens and immune complexes were determined by enzyme-linked immunosorbent assays (ELISA). The anti-SiSV gp70 antiserum used predominantly recognized the protein moieties of the glycoproteins. The distribution of SiSV gp70-related antigens and immune complexes was similar among leukemic and non-leukemic sera. The prevalence of SiSV gp70-related antigens was 53% and of SiSV gp70-related immune complexes 49% in all sera. SiSV gp70-related antigens were detected in a somewhat higher proportion of non-leukemic (69%) than leukemic sera (40%), whereas SiSV gp70-related immune complexes and cross-reactive antibodies were more evenly distributed in leukemic and non-leukemic sera (in 46 and 51% of leukemic and 54 and 51% of non-leukemic sera). Presence of antigens correlated with presence of SiSV gp70-related immune complexes in 71% of all sera, but in 13% of all sera antigens were detectable only by determining SiSV gp70-related immune complexes. Total circulating immune complexes did not correlate with SiSV gp70-related immune complexes. The origin and pathophysiological role of the antigens are discussed.

Acute Disease↗
PubMed1984

HLA-D and -DR antigens on human amniotic fluid cells. II. Heterogeneous expression of HLA-DR and other cell surface markers.

To evaluate further the feasibility of HLA typing for prenatal diagnosis, we tested human amniotic fluid cells (AFC), known to express HLA-A, -B, and -C antigens, for the presence of HLA-DR antigens using type-specific antisera in the microcytotoxicity assay and a monoclonal antibody directed against the common HLA-DR structure (cDR) in indirect immunofluorescence. Prenatal typing of HLA-DR on AFC in the microcytotoxicity test was possible in only one out of eight families studied. The detected DR2 antigen was confirmed by postnatal typings of cord blood lymphocytes. Thereafter, 23 different AFC cultures were tested with monoclonal antibodies in indirect immunofluorescence. Only six cultures were partially positive (23-35% fluorescent cells) with the monoclonal cDR antibody while all AFC cultures demonstrated strong positive fluorescence (68-100%) with a monoclonal antibody against the common HLA-A, -B, and -C structure (cHLA). These data suggest that only a small subpopulation of AFC expresses class II (HLA-DR) antigens in contrast to the nearly ubiquitous expression of class I (HLA-A, -B, and -C) antigens. Furthermore, the heterogeneous expression of cell surface antigens within the various AFC cultures was substantiated with monoclonal antibodies directed toward cell surface antigens of the OKT, OKM, and Lyt series that have been found to be characteristic for subpopulations of lymphoid and hemapoetic cells. Thus, at present, HLA-DR typing is not reliable for prenatal diagnosis.

Amniotic Fluid↗
PubMed1983

RNA-tumorviruses, oncogenes, and their possible role in human carcinogenesis.

The detection and characterization of oncogenes via RNA tumor viruses (or retroviruses) and the recognition of their location at breakpoints of chromosomal translocations which are frequently found in certain human neoplasms has promoted present understanding of molecular mechanisms underlying carcinogenesis. Oncogenes are cellular genes which can be transduced by RNA tumorviruses and induce malignant transformation under experimental conditions in vivo and in vitro. A role of retroviruses in human leukemogenesis is suggested by epidemiological observations and by the isolation of such viruses from several human T-cell leukemias and lymphomas (human T-cell leukemia/lymphoma virus or HTLV) as well as by biochemical association of retroviral markers with human leukemias. A role of HTLV has been suggested also in a human immune deficiency syndrome (AIDS). In view of the well known role of many factors in carcinogenesis the concept of carcinogenesis as a multistep process as well as the concept of cocarcinogenesis and the role of cofactors other than viruses, such as radiation and chemicals, aging, hormones, graft vs host reaction, environmental factors etc., will have to be carefully considered.

Acquired Immunodeficiency Syndrome↗
PubMed1983

[Immunogenetics of myasthenia gravis. Significance of HLA-, complement and Cm gene systems for clinical and immunologic parameters].

In 82 non-related patients with myasthenia gravis the following immunogenetic marker systems were investigated: HLA-A, -B, -C, -DR antigens, complement polymorphisms for Bf, C3 and C4 as well as immunoglobulin allotypes G1m, G3m and Km. In 78 patients the level of circulating acetylcholin receptor autoantibody was measured. The HLA antigens showed no significant differences in frequency when compared with healthy controls. This was also true for the HLA-bound Bf and C4 polymorphism, the non-HLA-bound C3 polymorphism and the immunoglobulin allotypes. A significant (P less than 0.005) increase in heterozygote frequency of 39.7% in the Gm allotype combination G1m (1), (17); (3) when compared with an expected frequency as calculated from the gene frequency of 19.8% was found. HLA-B8 and/or HLA-DR3 positive myasthenia gravis patients showed a significantly (P less than 0.025 and less than 0.005) earlier average onset of the disease whereas in HLA-DR2 positive patients the average onset was later (P less than 0.05). The same HLA antigens correlated with quantitative differences in the acetylcholine receptor autoantibodies: HLA-B8 and/or -DR3 positive patients had on average higher antibody levels than HLA-B8 or -DR3-negative patients. The difference for HLA-DR3 was statistically significant (P less than 0.05). On the other hand patients with HLA-DR2 antigens had significantly lower antibody levels (P less than 0.025). Increased mean antibody levels were also seen in G1m(1), (17) allotype (P less than 0.005) and G3m(21) (P less than 0.05). As the HLA antigens and Gm allotype genes are situated on different chromosomes (C6 and C14) two distinct gene regions are identified in myasthenia gravis. These are associated with quantitative differences in acetylcholine receptor antibody titres.

Autoantibodies↗
PubMed1983

HLA-D and -DR antigens on human amniotic fluid cells. I. Lack of expression of HLA-D.

Human amniotic fluid cells, known to express HLA-A, -B, and -C antigens, were tested for the presence of lymphocyte-stimulating antigens (LD or HLA-D) using modifications of the mixed lymphocyte culture (MLC) and primed lymphocyte typing (PLT) tests. Peripheral blood lymphocytes were co-cultured with various concentrations of allogeneic amniotic fluid cells, either growing as a monolayer culture in microtiter plates or suspended in medium following treatment with trypsin. The kinetics of such mixed lymphocyte amniotic fluid cell culture (MLAC) reactions were followed during days 3 to 8. Under none of these conditions did amniotic fluid cells significantly stimulate allogeneic lymphocytes, even after lymphocytes were specifically primed in the PLT assay to the HLA-D antigens segregating in the family of the amniotic fluid cell donor. Furthermore, in three-cell experiments, amniotic fluid cells failed to inhibit an ongoing MLC reaction, indicating that the absence of proliferative response to amniotic fluid cells is not due to active suppression. Taken together, these data strongly suggest that amniotic fluid cells either do not express HLA-D antigens or do not express them in a form that is detectable in either primary or secondary MLC.

Amniotic Fluid↗
PubMed1981

Suppression of the generation of secondary virus-specific proliferative and cytotoxic T lymphocytes by suppressor cells induced during primary anti-viral sensitization in vitro.

Murine spleen cells first primed with syngeneic vaccinia virus-infected peritoneal exudate cells (PEC) in vitro and then restimulated with the virus failed to give a typical virus-specific secondary cytotoxic T lymphocyte (CTL) response. In contrast, "memory' spleen cells from mice primed with the virus in vivo produced CTL after the same challenge with virus-infected PEC in vitro. In the former situation, the lack of a virus-specific secondary CTL response by in vitro primed and restimulated spleen cells seemed to be associated with the generation of suppressor cells in cultures; these cells inhibited the cytotoxic as well as proliferative secondary and tertiary responses of spleen presensitized with virus in vitro alone, or in vivo plus in vitro. Weak suppressor activity was also induced in control spleen-cell cultures from normal unprimed or virus-primed mice that were not stimulated with virus-infected cells, suggesting either a quantitative difference in the generation of suppression or, alternatively, the co-existence of virus-dependent and independent suppressor cells in the virus-stimulated cultures. Our experiments cannot conclusively establish that suppression is T-cell mediated and/or possibly natural-killer-(NK)-cell dependent. The suppressor phenomena were exerted by irradiation resistant (850 rad) lymphocytes that passed through nylon wool columns and were sensitive to treatment with anti-Thy-1 antibody plus C; but the suppressor cells were partially reactive across allogeneic barriers.

Animals↗
PubMed1978

Ir-genes in H-2 regulate generation of anti-viral cytotoxic T cells. Mapping to K or D and dominance of unresponsiveness.

H-2 dependent and virus-specific Ir genes regulate the generation of primary virus-specific K or D restricted cytotoxic T-cell responses in vivo. The following examples have been analyzed in some detail: first, Dk restricted responses to vaccinia in Sendai viruses are at least 30 times lower than the corresponding K-restricted responses irrespective of the H-2 haplotypes (k, b, d, dxs, dxq) of K and I regions; in contrast, LCMV infection generates high responses to Dk. These findings are consistent with but do not prove that this Ir gene maps to D. Second, Db restricted responses to vaccinia and Sendai viruses are high in strains possessing the Kq or KbIb, KbaIb haplotype, are very low in strains with Kk, and relatively low in mouse strains of the KdI-Ad haplotype; LCMV generates high Db restricted response in the presence of Kk. This Ir gene for the response to vaccinia and Sendai viruses maps to K since B10.BYR (KqIkdDb) is a responder and B10.A (2R) is a nonresponder (KkIkdDb). Third, virus and K or D allele specific nonresponsiveness is dominant with variable penetrance; in heterozygous mice the nonresponder Kk allele over-rides responsiveness normally found in KbDb or KqDb combinations. Fourth, when (responder X nonresponder)F1 lymphocytes are stimulated in an environment expressing vaccinia virus plus only a high responder Kb or Kq allelle and Db, response to vaccinia Db is high; in contrast when the same F1 cells are stimulated in an environment expressing the low responder allele Kk, response to vaccinia Db is low. Thus absence of Kk during immunization allows generation of high responsive Db restricted vaccinia specific cytotoxic T cells. The Dk dependent low response to vaccinia Dk can be explained by a preclusion rule or by failure of vaccinia to complex with Db; however the analysis of Kk dependent low response to vaccinia Db does not support these explanations or that self-tolerance is responsible for this Ir effect but is compatible with the interpretation that Kk vaccinia is immunodominant over Db vaccinia. These results are discussed with respect to (a) possible mechanisms of regulation by Ir genes and (b) H-2 polymorphism and HLA-disease association.

Alleles↗