The pathogenesis of transmissible spongiform encephalopathies (TSEs) often includes a replication phase in lymphoid tissues before infection spreads to the central nervous system. Recent studies show that the follicular dendritic cells of the germinal centres are critical for this replication. These cells are therefore potential targets for therapy or prophylaxis in natural TSEs, such as variant Creutzfeldt-Jakob disease.
Until recently, the relationship between apoptosis, selection in the germinal centre (GC) and production of high-affinity antibody-forming cells (AFCs) and memory B cells has been unclear. Here, Tarlinton and Smith present a model that accounts for the switch in GC production from high-affinity AFCs to memory B cells, and explain how Bcl-2, an inhibitor of apoptosis, can influence memory cells but not bone marrow AFCs.
Defects in the major histocompatibility complex (MHC) class I antigen-processing machinery (APM) have been described in tumors of different histology. Murine data suggest that defects in the MHC class II APM might also be associated with malignant transformation of human cells. This article describes the pathophysiology of the MHC class I and II APM, reviews APM abnormalities in tumor cells and discusses their role in the escape of tumor cells from in vitro recognition by T cells.
Evidence presented at a recent conference* indicated that dendritic cells should be regarded as a multi-lineage system of leukocytes with variable function rather than a homogenous cell type with predetermined functional properties.
Natural killer (NK) cells have often been regarded as somewhat ‘primitive’ and ‘nonspecific’; however, new data have revealed an unexpected complexity and a sophisticated capability of detecting potentially dangerous cells.
This short article highlights the principal elements of a lecture that will be delivered by Rolf M. Zinkernagel at EFIS 2000 in Poland.
An improved understanding of cell biology, genetics, and molecular and developmental biology, together with an appreciation of the fact that immunity is the result of coevolution, are leading to a better understanding of the rules and exceptions of immunity.
During the millions of years they have coexisted with their hosts, viruses have learned how to manipulate host immune control mechanisms. Viral gene functions provide an overview of many relevant principles in cell biology and immunology. Our knowledge of viral gene functions must be integrated into virus–host interaction networks to understand viral pathogenesis, and could lead to new anti-viral strategies and the ability to exploit viral functions as tools in medicine.
By examining immunoglobulin (Ig) and T-cell receptor (TCR) gene loci and their rearrangement patterns in many species, and by imposing evolutionary principles, we can determine fundamentals regarding the behavior and properties of recognitive repertoires. A recent meeting* addressed the opposing selection pressures that determine the size of the repertoire, the characterization of specificity and the rules for effector function.
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