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R Riese

Publications and source records attributed to R Riese.

5 recordsLinked to original sources

Developmental plasticity of CNS microglia.

Microglia arise from CD45(+) bone marrow precursors that colonize the fetal brain and play a key role in central nervous system inflammatory conditions. We report that parenchymal microglia are uncommitted myeloid progenitors of immature dendritic cells and macrophages by several criteria, including surface expression of "empty" class II MHC protein and their cysteine protease (cathepsin) profile. Microglia express receptors for stem cell factor and can be skewed toward more dendritic cell or macrophage-like profiles in response to the lineage growth factors granulocyte/macrophage colony-stimulating factor or macrophage colony-stimulating factor. Thus, in contrast to other organs, where terminally differentiated populations of resident dendritic cells and/or macrophages outnumber colonizing precursors, the majority of microglia within the brain remain in an undifferentiated state.

Animals↗

Role for cathepsin F in invariant chain processing and major histocompatibility complex class II peptide loading by macrophages.

The major histocompatibility complex (MHC) class II-associated invariant chain (Ii) regulates intracellular trafficking and peptide loading of MHC class II molecules. Such loading occurs after endosomal degradation of the invariant chain to a approximately 3-kD peptide termed CLIP (class II-associated invariant chain peptide). Cathepsins L and S have both been implicated in degradation of Ii to CLIP in thymus and peripheral lymphoid organs, respectively. However, macrophages from mice deficient in both cathepsins S and L can process Ii and load peptides onto MHC class II dimers normally. Both processes are blocked by a cysteine protease inhibitor, indicating the involvement of an additional Ii-processing enzyme(s). Comparison of cysteine proteases expressed by macrophages with those found in splenocytes and dendritic cells revealed two enzymes expressed exclusively in macrophages, cathepsins Z and F. Recombinant cathepsin Z did not generate CLIP from Ii-MHC class II complexes, whereas cathepsin F was as efficient as cathepsin S in CLIP generation. Inhibition of cathepsin F activity and MHC class II peptide loading by macrophages exhibited similar specificity and activity profiles. These experiments show that cathepsin F, in a subset of antigen presenting cells (APCs), can efficiently degrade Ii. Different APCs can thus use distinct proteases to mediate MHC class II maturation and peptide loading.

Animals↗

Cathepsin S required for normal MHC class II peptide loading and germinal center development.

Major histocompatibility complex (MHC) class II molecules acquire antigenic peptides after degradation of the invariant chain (Ii), an MHC class II-associated protein that otherwise blocks peptide binding. Antigen-presenting cells of mice that lack the protease cathepsin S fail to process Ii beyond a 10 kDa fragment, resulting in delayed peptide loading and accumulation of cell surface MHC class II/10 kDa Ii complexes. Although cathepsin S-deficient mice have normal numbers of B and T cells and normal IgE responses, they show markedly impaired antibody class switching to IgG2a and IgG3. These results indicate cathepsin S is a major Ii-processing enzyme in splenocytes and dendritic cells. Its role in humoral immunity critically depends on how antigens access the immune system.

Animals↗

Crystal-cell interactions: crystal binding to rat renal papillary tip collecting duct cells in culture.

Retention of stone crystallites by urothelium is clearly one of the prime requisites for urinary stone disease. Studies in the literature as early as 1937 have highlighted that the initiation of renal calculi followed the formation of subepithelial calcified plaques in the renal pelvis. The renal papilla is one of the primary sites for crystal fixation and stone maturation. We have developed an in vitro model system for the study of kidney stone crystal retention to tubular epithelium using rat renal papillary collecting tubule (RPCT) cells in primary culture. We have qualitatively and quantitatively analyzed the binding of preformed calcium oxalate monohydrate (COM), hydroxyapatite (HA), and uric acid (UA) crystals to RPCT cells. Our goal was to determine if three common urinary stone crystals evidenced different crystal-cell binding characteristics. Also, since these crystals are frequently observed admixed in stones, we have studied the inhibitive binding characteristics of these crystals with RPCT cells. The RPCT cells in culture grow both as the typical polygonal cells in monolayer and as clumps of aggregated cells. The cells in the aggregates are viable epithelial cells that have lost their attachment to the basement membrane, resulting in the exposure of surface molecules that would not normally be present unless the cells were damaged or if there was a loss of intercellular tight junctions. COM, HA, and UA crystals all preferentially bound to the aggregated cells and all exhibited similar saturable binding patterns.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Multidisciplinary team functioning.

This paper advocates the need to move beyond interdisciplinary team composition as a minimum criterion for multidisciplinary functioning in child abuse treatment. Recent developments within the field reflect the practice of shared professional responsibility for detection, case management and treatment. Adherence to this particular model for intervention requires cooperative service planning and implementation as task related functions. Implicitly, this model also carries the potential to incorporate the supportive functioning essential to effective group process. However, explicit attention to the dynamics and process of small groups has been neglected in prescriptive accounts of multidisciplinary child abuse team organization. The present paper therefore focuses upon the maintenance and enhancement aspects of multidisciplinary group functioning. First, the development and philosophy of service for the Alberta Children's Hospital Child Abuse Program are reviewed. Second, composition of the team, it's mandate for service, and the population it serves are briefly described. Third, the conceptual framework within which the program functions is outlined. Strategies for effective group functioning are presented and the difficulties encountered with this model are highlighted. Finally, recommendations are offered for planning and implementing a multidisciplinary child abuse team and for maintaining its effective group functioning.

Child Abuse↗