Death of mature T cells by separate ligation of CD4 and the T-cell receptor for antigen

Article Abstract:

While the recognition of antigens by antibodies is a one-on-one affair, and does not require accessory molecules, the recognition of antigen by the T-cell receptor is quite complex. To begin with, the T-cell antigen receptor only recognizes antigen which is properly presented in a complex with molecules of the major histocompatibility complex (MHC). Furthermore, the T-cell receptor functions on the surface of T cells in a complex with the CD3 cell surface molecule. Considerable controversy remains over the degree to which other cell-surface molecules may also be involved. It is known that CD4 recognizes class II molecules of the major histocompatibility complex, and it is proposed that CD4 plays a role in the initiation of the complex formation between the presented antigen and the T-cell receptor-CD3 complex. It is also known, however, that the "restriction" of the T-cell response, that is, the ability of T cells to recognize only those antigens presented by the proper "self" MHC antigens, does not require CD4. One way in which the contribution of different cell surface molecules may be determined is through the use of specific antibodies. Often, changes result when the cell surface molecule is ligated; that is, bound by antibodies to its peers on the cell surface. These molecules are no longer able to participate in their normal cell-surface functions. Such an experiment was performed on the CD4 molecule on the T-cell surface. When the CD4 molecules were ligated prior to stimulation of the T cell by antigen, the cells were unresponsive. This was found to be due to apoptosis of the T cells. Apoptosis is a physiologically normal cell death which results when the cell cleaves its own DNA into pieces. Apoptosis is one mechanism for eliminating cells which no longer serve the body's purpose. The demonstration of apoptosis following CD4 ligation and antigen stimulation suggests that CD4 plays a key role in the normal response of the cells to antigen. The authors suggest that it may also provide some insight into why the T-cell response must be restricted to the proper MHC presentation to begin with. (Consumer Summary produced by Reliance Medical Information, Inc.)

Cell death, HLA histocompatibility antigens

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Competition for antigen presentation in living cells involves exchange of peptides bound by class II MHC molecules

Article Abstract:

The body's natural defense system, the immune system, consists of cells and factors that inactivate invading foreign particles called antigens. In the presence of an antigen, the immune B cells produce specialized proteins called antibodies that specifically bind and inactivate that antigen. There are three types of immune T cells: helper T cells increase antibody production by B cells; suppressor T cells decrease antibody production by B cells; and killer T cells interact with antigens present on foreign cells and are capable of destroying these foreign cells. Killer T cells may also act against the histocompatibility antigens of other individuals within the same species. These histocompatibility antigens are present on all cells with a nucleus and are important in transplantation reactions; they are controlled by a group of genes called the major histocompatibility gene complex (MHC). T cells recognize foreign proteins as peptides or short proteins, that are bound to MHC-controlled molecules. The binding of these peptides to the MHC-controlled molecules is slow but stable. Results from this study show that there is an exchange of peptides between the binding sites on MHC-controlled molecules. (Consumer Summary produced by Reliance Medical Information, Inc.)

Medical examination, Histocompatibility antigens

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Phagocytic processing of bacterial antigens for class I MHC presentation to T cells

Article Abstract:

A new mechanism for the phagocytic processing of bacterial antigens by class I major histocompatibility complex I molecules has been discovered. This mechanism, which works for antigens lacking cytosolic penetration, produces resistance to the drugs cycloheximide and Brefeldin A. In contrast, these drugs are able to inhibit the classical class I pathway. This pathway may allow CD8 T-cells to be used against intracellular pathogens.

Phagocytosis, Bacterial antigens, O antigens

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