Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renal proximal tubule (PT) in many ways resembles an APC. The PT is one of the few epithelial cells in the body reported to constitutively express the class II MHC molecules required to present Ag to CD4+ T cells. We questioned whether the PT could function as an APC in vitro and in vivo. Fluorescence cytometry demonstrated that the normal CBA/J PT constitutively expressed low levels of class II MHC and that this expression was markedly augmented by either IFN-gamma or systemic Listeria monocytogenes infection. Functionally, the PT from normal CBA/J mice also stimulated T cell hybridomas when cultured in vitro with Ag, and this ability was markedly up-regulated by both IFN-gamma as well as L. monocytogenes infection. To prove that the PT constitutively processed and presented self Ag in vivo, freshly isolated PT from mice transgenic for human alpha 1-antitrypsin were cultured with the appropriate T cell hybridoma in the absence of exogenous Ag. Strong stimulation of the T cell hybridoma occurred. Our data show that the renal proximal tubule processes and presents foreign Ag both in vitro and in vivo, and that it constitutively processes and presents the self Ag hAAT in vivo. These results have important implications for the understanding of renal interstitial autoimmune diseases as well as the interstitial nephritis that occurs in response to foreign Ag.
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PMID:Processing and presentation of self and foreign antigens by the renal proximal tubule. 156 Jan 95

Protection against intracellular bacteria by T cells is regulated by Ag-presenting molecules, which comprise classical MHC class I molecules, MHC class II molecules, and nonclassical MHC class Ib molecules. The role of CD1 molecules, which are structurally similar to classical MHC class I gene products, but less polymorphic, is not understood so far. We show that CD1 surface expression increased on APC in Listeria-infected mice. The in vivo treatment with anti-CD1 mAb reduced TGF-beta 2 levels and concomitantly increased secretion of the proinflammatory cytokine TNF, the Th1 cell promoting cytokine IL-12, and the Th1 cell cytokine IFN-gamma at the onset of listerial infection. These findings point to a regulatory role of CD1-reactive cells in the immune response against listeriosis.
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PMID:Cutting edge: anti-CD1 monoclonal antibody treatment reverses the production patterns of TGF-beta 2 and Th1 cytokines and ameliorates listeriosis in mice. 1035 32

The immunologic requirements for generating long-lived protective CD8 T cell memory remain unclear. Memory CD8 populations generated in the absence of CD4 Th cells reportedly have functional defects, and at least a subset of CD8 T cells transiently express CD40 after activation, suggesting that direct CD4-CD8 T cell interactions through CD40 may influence the magnitude and functional quality of memory CD8 populations. To ascertain the role of CD40 in such direct T cell interactions, we investigated CD8 T cell responses in CD40-/- mice after infection with Listeria monocytogenes, an intracellular bacterium that induces APC activation and thus priming of CD8 T cells independently of CD4 Th cell help through CD40. In this study we show that memory CD8 T cells generated in CD40-deficient mice show in vivo cytotoxicity and cytokine production equivalent to CD8 memory T cells from wild-type mice. Upon secondary Listeria infection, CD40-/- memory CD8 T cells expand to greater numbers than seen in wild-type mice. These results indicate that CD40 ligation on CD8 T cells, although reportedly a part of CD8 T cell memory development in an H-Y-directed response, is not needed for the development of functional memory CD8 T cell populations after Listeria infection.
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PMID:The development of functional CD8 T cell memory after Listeria monocytogenes infection is not dependent on CD40. 1535 58

Regulation of CD8 T cell expansion and contraction is essential for successful immune defense against intracellular pathogens. IL-10 is a regulatory cytokine that can restrict T cell responses by inhibiting APC functions. IL-10, however, can also have direct effects on T cells. Although blockade or genetic deletion of IL-10 enhances T cell-mediated resistance to infections, the extent to which IL-10 limits in vivo APC function or T cell activation/proliferation remains unknown. Herein, we demonstrate that primary and memory CD8 T cell responses following Listeria monocytogenes infection are enhanced by the absence of IL-10. Surface expression of the IL-10R is transiently up-regulated on CD8 T cells following activation, suggesting that activated T cells can respond to IL-10 directly. Consistent with this notion, CD8 T cells lacking IL-10R2 underwent greater expansion than wild-type T cells upon L. monocytogenes infection. The absence of IL-10R2 on APCs, in contrast, did not enhance T cell responses following infection. Our studies demonstrate that IL-10 produced during bacterial infection directly limits expansion of pathogen-specific CD8 T cells and reveal an extrinsic regulatory mechanism that modulates the magnitude of memory T cell responses.
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PMID:Pathogen-specific CD8 T cell responses are directly inhibited by IL-10. 1787 48