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G. G. B. Klaus

Bio: G. G. B. Klaus is an academic researcher. The author has contributed to research in topics: Antigen & T cell. The author has an hindex of 1, co-authored 1 publications receiving 185 citations.

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01 Jan 1987
TL;DR: The induction and enumeration of antibody-forming cells in vitro and the development of human B lymphoblastoid cell lines using epstein are studied.
Abstract: Preparation of lymphocytes and accessory cells Preparation of lymphocyte subpopulations Fractionation of lymphocytes by immunomagnetic beads Immunofluorescence and immunohisto-chemistry The induction and enumeration of antibody-forming cells in vitro In vitro culture of T cell lines and clones Generation of human B lymphoblastoid cell lines using epstein Limiting dilution analysis Lymphocyte proliferation assays Assays for interleukins and other related factors Biochemical characterization of lymphocyte surface antigens

185 citations


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Journal ArticleDOI
TL;DR: It is demonstrated that OX40-OX40L interactions control primary T cell expansion and the ability to retain high numbers of Ag-specific T cells and can promote survival of greater numbers of T cells with time and control the size of the memory T cell pool.
Abstract: The costimulatory receptor OX40 has recently been shown to be involved in primary CD4 responses to several defined Ags. However, to date there has been little information regarding the mechanism of action of OX40, such as whether it regulates T cell numbers, reactivity, or both, and whether it contributes to induction of long-term T cell responses. With an agonist Ab to OX40, and by tracking Ag-specific TCR transgenic T cells in vivo, we show that ligation of OX40 induces clonal expansion and survival of CD4 cells during primary responses, and results in the accumulation of greater numbers of memory cells with time. Significantly, OX40-deficient T cells, from mice generated by gene targeting, secrete IL-2 and proliferate normally during the initial period of activation, but cannot sustain this during the latter phases of the primary response, exhibiting decreased survival over time. Mice lacking OX40 develop only low frequencies of Ag-specific CD4 cells late in primary responses in vivo and generate dramatically lower frequencies of surviving memory cells. These results demonstrate that OX40-OX40L interactions control primary T cell expansion and the ability to retain high numbers of Ag-specific T cells. In this way, OX40 signals promote survival of greater numbers of T cells with time and control the size of the memory T cell pool.

402 citations

Journal ArticleDOI
TL;DR: It is revealed that in the thymus the regulatory cells are observed in the CD25+ subset of CD4+CD8− cells, whereas transfer of the corresponding CD25− thymocyte subset leads to acceleration of disease onset in prediabetic recipients.
Abstract: Previously we have shown that autoimmune diabetes, induced in rats by a protocol of adult thymectomy and split-dose gamma irradiation, can be prevented by the transfer of a subset of CD4+ T cells with a memory phenotype (CD45RC-), as well as by CD4+CD8- thymocytes, from syngeneic donors Further studies now reveal that in the thymus the regulatory cells are observed in the CD25+ subset of CD4+CD8- cells, whereas transfer of the corresponding CD25- thymocyte subset leads to acceleration of disease onset in prediabetic recipients However, in the periphery, not all regulatory T cells were found to be CD25+ In thoracic duct lymph, cells that could prevent diabetes were found in both CD25- and CD25+ subsets of CD4+CD45RC- cells Further, CD25- regulatory T cells were also present within the CD4+CD45RC- cell subset from spleen and lymph nodes, but were effective in preventing diabetes only after the removal of CD25- recent thymic emigrants Phenotypic analysis of human thymocytes showed the presence of CD25+ cells in the same proportions as in rat thymus The possible developmental relationship between CD25+ and CD25- regulatory T cells is discussed

336 citations

Journal ArticleDOI
TL;DR: The pattern of infection observed in MHV-68-infected mice is similar to that seen in infectious mononucleosis of man following Epstein-Barr virus infection, and may prove to be useful in studying natural gamma-herpesvirus infections of man and domestic animals.
Abstract: The primary infection of BALB/c mice with murine herpesvirus 68 (MHV-68) was investigated. When the virus was introduced intranasally, the lung was the main tissue infected, the virus being associated with alveolar epithelium and mononuclear cells. A productive infection lasted for 10 days, after which viral DNA could be detected by in situ hybridization up to 30 days after infection. At that time lymphoproliferative accumulations were also observed in the lung, with formation of germinal centres. Virus could also be recovered from the heart, kidney, adrenal gland and spleen during the primary infection. In addition, the spleen appeared to be the major site of virus persistence, with latently infected cells detected up to 90 days post-infection. During the primary infection, there was atrophy of the thymus and spleen of clinically sick animals. In contrast, lymphoproliferative responses, typified by splenomegaly, were frequently seen in asymptomatic animals. The pattern of infection observed in MHV-68-infected mice is similar to that seen in infectious mononucleosis of man following Epstein—Barr virus infection. The model described in this paper may prove to be useful in studying natural gamma-herpesvirus infections of man and domestic animals.

324 citations

Journal ArticleDOI
TL;DR: It is concluded that both genetic variation and epigenetic modifications contribute to the regulation of SLC6A4 function and that more in‐depth studies of the molecular mechanisms controlling gene activity and the relationship of these mechanisms to behavioral illness are indicated.
Abstract: Serotonin Transporter (5HTTor SLC6A4) mRNA transcription is regulated by both genetic and epigenetic mechanisms. Unfortunately, despite intense scrutiny, the exact identity and contribution of each of these regulatory mechanisms, and their relationship to behavioral illness remain unknown. This lack of knowledge is critical because alterations in SLC6A4 function are posited to be central to a wide variety of CNS disorders. In order to address this shortcoming, we quantified 5HTTLPR genotype, SLC6A4 mRNA production and CpG methylation using biomaterial from 192 lymphoblast cell lines derived from subjects who participated in the latest wave of the Iowa Adoption Studies. We then analyzed the resulting data with respect to clinical characteristics. We confirmed prior findings that the short (s) 5HTTLPR allele is associated with lower amounts of mRNA transcription, but there was no significant effect of the “Long G” allele on mRNA transcription. We also found that CpG methylation was higher (P< 0.0008) and mRNA production (P< 0.0001) was lower in females as compared to males. Those subjects with a lifetime history of Alcohol Dependence had higher levels of SLC6A4 mRNA. There was a trend for an association of increased overall methylation with lifetime history of major depression. Finally, we confirm our prior findings that the exact levels of 5HTT mRNA expression are dependent on how it is measured. We conclude that both genetic variation and epigenetic modifications contribute to the regulation of SLC6A4 function and that more in-depth studies of the molecular mechanisms controlling gene activity and the relationship of these mechanisms to behavioral illness are indicated.

285 citations