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C Baan

Publications and source records attributed to C Baan.

6 recordsLinked to original sources
PubMed2006

FoxP3+ T cells can be expanded from rejecting cardiac allografts.

A specific subset of T cells, the FoxP3+ regulatory T cells, control effector T-cell responses to self and foreign antigens. In transplant patients, we and others have shown that high intragraft FOXP3 mRNA levels are associated with acute rejection, suggesting that immune regulation is dependent on immune activation. To study whether transplanted grafts harbor FoxP3+ T cells and to functionally analyze them, graft infiltrating lymphocytes (GILs) must be propagated from the transplanted tissue. In the present study, we analyzed whether FoxP3+ T cells can be grown from endomyocardial biopsies (EMBs; n = 5) from patients after heart transplantation during acute cellular rejection. After 18 to 21 days of culture, 0.5 to 1.0 x 10(6) GILs were cultured from the EMBs. Of these GILs, 10.6% (median; range, 1.6%-17.1%) stained positive for FoxP3. Thus Foxp3+ T cells can be grown from EMBs, providing the tools to functionally characterize these cells in depth in forthcoming studies.

Forkhead Transcription Factors↗
PubMed1994

Cytokine gene expression profiles in human endomyocardial biopsy (EMB) derived lymphocyte cultures and in EMB tissue.

The reverse transcriptase polymerase chain reaction (RT-PCR) technique was used to analyse cytokine gene expression in relation to acute cardiac rejection. Expression of interleukins, IL-2, IL-4, IL-6 and IL-10 mRNA was studied in sequential endomyocardial biopsies (EMB) and in graft-infiltrating lymphocyte (GIL) cultures propagated from EMB taken after heart transplantation. The cytokine gene expression of GIL propagated from EMB taken during an episode of rejection and of immunological quiescence was comparable. In contrast, posttransplant EMB showed selective IL-2 gene expression when rejection was diagnosed. IL-4 mRNA was absent in pretransplant EMB but present in posttransplant EMB taken during periods of rejection and of immunological quiescence. Both IL-6 and IL-10 transcripts were found in pre- and posttransplant EMB. These findings confirmed that IL-2 is specifically involved in cardiac rejection, while IL-4 may play a role in immune responses leading to graft rejection or graft tolerance.

Biopsy↗
PubMed1988

Genetic complementation analysis of ataxia telangiectasia and Nijmegen breakage syndrome: a survey of 50 patients.

Cultured cells from patients with ataxia telangiectasia (AT) or Nijmegen breakage syndrome (NBS) are hypersensitive to ionizing radiation. After radiation exposure, the rate of DNA replication is inhibited to a lesser extent than in normal cells, whereas the frequency of chromosomal aberrations is enhanced. Both of these features have been used in genetic complementation studies on a limited series of patients. Here we report the results of extended complementation studies on fibroblast strains from 50 patients from widely different origins, using the radioresistant DNA replication characteristic as a marker. Six different genetic complementation groups were identified. Four of these, called AB, C, D, and E (of which AB is the largest), represent patients with clinical signs of AT. Patients having NBS fall into two groups, V1 and V2. An individual with clinical symptoms of both AT and NBS was found in group V2, indicating that the two disorders are closely related. In AT, any group-specific patterns with respect to clinical characteristics or ethnic origin were not apparent. In addition to the radiosensitive ATs, a separate category of patients exists, characterized by a relatively mild clinical course and weak radiosensitivity. It is concluded that a defect in one of at least six different genes may underlie inherited radiosensitivity in humans. To facilitate research on defined defects, a complete list of genetically characterized fibroblast strains is presented.

Ataxia Telangiectasia↗
PubMed1988

A new chromosomal instability disorder confirmed by complementation studies.

Two sisters with a complex clinical pattern, including microcephaly, microgenia, defects of skin pigmentation, anal stenosis/atresia, and combined immunodeficiency together with spontaneous chromosomal instability and cellular hypersensitivity to X-rays and bleomycin are described. Complementation studies on heterokaryons proved that the underlying genetic defect is non-allelic with that of patients with ataxia telangiectasia (complementation groups AB-E) and the Nijmegen breakage syndrome, but identical with the case described by Conley et al. (1986).

Ataxia Telangiectasia↗
PubMed1988

Patients with an inherited syndrome characterized by immunodeficiency, microcephaly, and chromosomal instability: genetic relationship to ataxia telangiectasia.

Fibroblast cultures from six unrelated patients having a familial type of immunodeficiency combined with microcephaly, developmental delay, and chromosomal instability were studied with respect to their response to ionizing radiation. The cells from five of them resembled those from individuals with ataxia telangiectasia (AT) in that they were two to three times more radiosensitive on the basis of clonogenic cell survival. In addition, after exposure to either X-rays or bleomycin, they showed an inhibition of DNA replication that was less pronounced than that in normal cells and characteristic of AT fibroblasts. However, the patients are clinically very different from AT patients, not showing any signs of neurocutaneous symptoms. Genetic complementation studies in fused cells, with the radioresistant DNA synthesis used as a marker, showed that the patients' cells could complement representatives of all presently known AT complementation groups. Furthermore, they were shown to constitute a genetically heterogeneous group as well. It is concluded that these patients are similar to AT patients with respect to cytological parameters. The clinical differences between these patients and AT patients are a reflection of genetic heterogeneity. The data indicate that the patients suffer from a chromosome-instability syndrome that is distinct from AT.

Ataxia Telangiectasia↗