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      Immunobiology of Dendritic Cells

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          Abstract

          Dendritic cells (DCs) are antigen-presenting cells with a unique ability to induce primary immune responses. DCs capture and transfer information from the outside world to the cells of the adaptive immune system. DCs are not only critical for the induction of primary immune responses, but may also be important for the induction of immunological tolerance, as well as for the regulation of the type of T cell-mediated immune response. Although our understanding of DC biology is still in its infancy, we are now beginning to use DC-based immunotherapy protocols to elicit immunity against cancer and infectious diseases.

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          T-cell help for cytotoxic T lymphocytes is mediated by CD40-CD40L interactions.

          S. P. Schoenberger, R Toes, E van der Voort … (1998)
          Although in vivo priming of CD8+ cytotoxic T lymphocytes (CTLs) generally requires the participation of CD4+ T-helper lymphocytes, the nature of the 'help' provided to CTLs is unknown. One widely held view is that help for CTLs is mediated by cytokines produced by T-helper cells activated in proximity to the CTL precursor at the surface of an antigen-presenting cell (APC). An alternative theory is that, rather than being directly supplied to the CTL by the helper cell, help is delivered through activation of the APC, which can then prime the CTL directly. CD40 and its ligand, CD40L, may activate the APC to allow CTL priming. CD40L is expressed on the surface of activated CD4+ T-helper cells and is involved in their activation and in the development of their effector functions. Ligation of CD40 on the surface of APCs such as dendritic cells, macrophages and B cells greatly increases their antigen-presentation and co-stimulatory capacity. Here we report that signalling through CD40 can replace CD4+ T-helper cells in priming of helper-dependent CD8+ CTL responses. Blockade of CD40L inhibits CTL priming; this inhibition is overcome by signalling through CD40. CD40-CD40L interactions are therefore vital in the delivery of T-cell help for CTL priming.
          Article 0 comments Cited 423 times – based on 0 reviews     Review now
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            Phylogenetic perspectives in innate immunity.

            J A Hoffmann, F C Kafatos, C A Janeway … (1999)
            The concept of innate immunity refers to the first-line host defense that serves to limit infection in the early hours after exposure to microorganisms. Recent data have highlighted similarities between pathogen recognition, signaling pathways, and effector mechanisms of innate immunity in Drosophila and mammals, pointing to a common ancestry of these defenses. In addition to its role in the early phase of defense, innate immunity in mammals appears to play a key role in stimulating the subsequent, clonal response of adaptive immunity.
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              A conditioned dendritic cell can be a temporal bridge between a CD4+ T-helper and a T-killer cell.

              J. P. Ridge, F. Di Rosa, P Matzinger (1998)
              To generate an immune response, antigen-specific T-helper and T-killer cells must find each other and, because they cannot detect each other's presence, they are brought together by an antigen-loaded dendritic cell that displays antigens to both. This three-cell interaction, however, seems nearly impossible because all three cell types are rare and migratory. Here we provide a potential solution to this conundrum. We found that the three cells need not meet simultaneously but that the helper cell can first engage and 'condition' the dendritic cell, which then becomes empowered to stimulate a killer cell. The first step (help) can be bypassed by modulation of the surface molecule CD40, or by viral infection of dendritic cells. These results may explain the long-standing paradoxical observation that responses to some viruses are helper-independent, and they evoke the possibility that dendritic cells may take on different functions in response to different conditioning signals.
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                Author and article information

                Journal
                Title: Annual Review of Immunology
                Abbreviated Title: Annu. Rev. Immunol.
                Publisher: Annual Reviews
                ISSN (Print): 0732-0582
                ISSN (Electronic): 1545-3278
                Publication date Created: April 2000
                Publication date (Print): April 2000
                Volume: 18
                Issue: 1
                Pages: 767-811
                Affiliations
                [1 ]Baylor Institute for Immunology Research, Dallas, Texas, 75204; email: , , ,
                [2 ]Laboratory of Immunological Research, Schering-Plough, Dardilly, 69572, France; email: , ,
                [3 ]Department of Immunobiology, DNAX Research Institute, Palo Alto, California, 94304; email:
                Article
                DOI: 10.1146/annurev.immunol.18.1.767
                PubMed ID: 10837075
                SO-VID: 66b7c45b-29da-45b2-943c-ebee5b40fd33
                Copyright © © 2000
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