ABSTRACT
BACKGROUND: People with mild intellectual disabilities (MID) experience more mental health (MH) problems than the general population but often do not receive appropriate primary MH care. Primary MH care is essential in integrative MH care and, therefore, demands high quality. To improve primary MH care for this patient group, account must be taken of the experiences of people with MID. So far, their perspectives have been largely absent from primary MH care research. OBJECTIVES: To explore patients' experiences, needs, and suggestions for improvement regarding primary MH care for people with MID. METHODS: Qualitative study among adults with MID who visited their GP with MH problems in the previous 12 months. Semi-structured interviews were conducted using a guide based on Person-Centred Primary Care Measures. Transcripts were analysed thematically. RESULTS: The 11 interviews that we conducted revealed four themes. The first theme, cumulative vulnerability, describes the vulnerability - instigated by the MID and reinforced by MH problems - experienced on a GP visit. The other themes (needs regarding the GP, needs regarding the network, self-determination) arise from this vulnerability. CONCLUSION: People with both MID and MH problems are extra vulnerable in primary care but desire self-determination regarding their MH care trajectory. This requires investment in a good GP-patient relationship and the organisation of additional support to meet these patients' needs, for which collaborative care with the patient, the patient's network, and other (care) professionals is of utmost importance.
People with mild intellectual disabilities (MID) feel more vulnerable visiting their GP with mental health (MH) problems than with somatic problemsPatients with MH problems report additional needs and expectations regarding their care and support networkGPs face challenges in coordinating care for patients with both MID and MH problems.
Subject(s)
Intellectual Disability , Interviews as Topic , Mental Health Services , Physician-Patient Relations , Primary Health Care , Qualitative Research , Humans , Male , Female , Intellectual Disability/therapy , Intellectual Disability/psychology , Adult , Middle Aged , Mental Health Services/organization & administration , Mental Disorders/therapy , Personal Autonomy , AgedABSTRACT
Thymic plasmacytoid dendritic cells (pDCs) are located predominantly in the medulla and at the corticomedullary junction, the entry site of bone marrow-derived multipotential precursor cells into the thymus, allowing for interactions between thymic pDCs and precursor cells. We demonstrate that in vitro-generated pDCs stimulated with CpG or virus impaired the development of human autologous CD34(+)CD1a(-) thymic progenitor cells into the T-cell lineage. Rescue by addition of neutralizing type I interferon (IFN) antibodies strongly implies that endogenously produced IFN-alpha/beta is responsible for this inhibitory effect. Consistent with this notion, we show that exogenously added IFN-alpha had a similar impact on IL-7- and Notch ligand-induced development of thymic CD34(+)CD1a(-) progenitor cells into T cells, because induction of CD1a, CD4, CD8, and TCR/CD3 surface expression and rearrangements of TCRbeta V-DJ gene segments were severely impaired. In addition, IL-7-induced proliferation but not survival of the developing thymic progenitor cells was strongly inhibited by IFN-alpha. It is evident from our data that IFN-alpha inhibits the IL-7R signal transduction pathway, although this could not be attributed to interference with either IL-7R proximal (STAT5, Akt/PKB, Erk1/2) or distal (p27(kip1), pRb) events.
Subject(s)
Cell Differentiation/physiology , Dendritic Cells/metabolism , Plasma Cells/metabolism , Stem Cells/metabolism , T-Lymphocytes/metabolism , Thymus Gland/metabolism , Animals , Antibodies/pharmacology , Antigens, CD/metabolism , Bone Marrow/metabolism , Cell Line , Coculture Techniques , Dendritic Cells/cytology , Humans , Interferon Type I/metabolism , Interleukin-7/metabolism , Mice , Plasma Cells/cytology , Protein Kinases/metabolism , Receptors, Antigen, T-Cell/metabolism , Receptors, Interleukin-7/metabolism , Signal Transduction/physiology , Stem Cells/cytology , T-Lymphocytes/cytology , Thymus Gland/cytologyABSTRACT
It is generally accepted that dendritic cells can be generated from either myeloid or lymphoid derived progenitors. Ample information has been collected on the development and nature of myeloid DC type 1 (DC1). In contrast, our current understanding on the origin and function of the lymphoid derived DC type 2 (DC2) is still limited but is increasing rapidly. Here we will summarize recent findings on the developmental origin of the precursor of DC2 (pre-DC2). The presence of pre-DC2 has been revealed in bone marrow, fetal liver, and cord blood, where they develop from hematopoietic stem cells (HSC) most likely via an intermediate pro-DC2 stage. Both in human and mouse, development of pre-DC2 depends on the cytokine FLT3-ligand (FLT3-L). In addition, transcription factors such as Spi-B and members of the basic helix-loop helix (bHLH) family have been shown to be involved in the proper differentiation of HSC into pre-DC2. The human thymus contains a population of cells that closely resembles the peripheral pre-DC2, including interferon (INF)-a production after viral stimulation. Some phenotypic differences have been observed however. Furthermore, we have shown that the thymic microenvironment is able to support development of pre-DC2 from HSC in vivo. A thymus independent pathway of pre-DC2 development exists as well, although at present it is not clear where these extrathymic pre-DC2 are generated. In regard of the absence of a phenotypic defined pro-DC2 population in the thymus, we speculate that development of thymic pre-DC2 may differ from peripheral pre-DC2. The challenge of the near future will be to determine the role of pre-DC2 during thymic T cell development.
