Article Abstract:
For antigens to be recognized by T cells, they must be presented in association with major histocompatibility (MHC) antigens, so that an immune response can be initiated. A B lymphocyte cell line, known as LBL 721.174, which has been mutated (changed genetically), is defective in that it cannot assemble or express class I MHC molecules on the cell surface. These cells were examined for defects in antigen presentation. The study showed that the cells could no longer present a viral antigen that is normally found inside of the virus which causes influenza, yet they could present a peptide that is normally found outside of the cell. Cells that expressed the class I antigens and cells that do not express the class I antigens were fused together and the characteristics of the progeny cells and the genes that were inherited by the progeny were studied. It was shown that the defect in antigen presentation was located on chromosome 6, where the MHC antigens are located. The gene involved in antigen presentation is different from the genes that code for the MHC antigens. The understanding of how antigen presentation occurs and the role of the molecules involved in the initiation of an immune response will allow further understanding and perhaps manipulation of the immune response so that an effective immune response may be induced against various foreign molecules, including viruses. (Consumer Summary produced by Reliance Medical Information, Inc.)
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Article Abstract:
Superantigens both aid and hinder the body's immunological defenses against infection by viruses such as the mouse mammary tumor retrovirus (MMTV). Superantigens strengthen the immune response by binding to class II major histocompatibility complex molecules, which in turn produce infection-fighting T cells with particular V-beta chains. However, superantigens also make T cells more vulnerable to infection by MMTV. The dual role of superantigens is prompting microbiologists and immunologists to collaborate in researching them.
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Article Abstract:
Mice lacking the hematopoietic transcription factor PU.1 exhibit arrested development of both osteoclasts and macrophages. Bones of PU.1-deficient mice failed to resorb cartilaginous bars and appositional bone and were devoid of osteoclasts, all of which are pathognomonic histological features of osteopetrosis. The absence of both osteoclasts and macrophages in PU.1-deficient mice indicates that the transcription factor may play a role in the initial stages of myeloid differentiation.
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