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Complex Cross-talk (complex + cross-talk)
Selected AbstractsImproving M cell mediated transport across mucosal barriers: do certain bacteria hold the keys?IMMUNOLOGY, Issue 1 2004Angela L. Man Summary Specialized microfold (M) cells of the follicle-associated epithelium (FAE) of the mucosal-associated lymphoid tissue (MALT) in gut and the respiratory system play an important role in the genesis of both mucosal and systemic immune responses by delivering antigenic substrate to the underlying lymphoid tissue where immune responses start. Although it has been shown that dendritic cells (DC) also have the ability to sample antigens directly from the gut lumen, M cells certainly remain the most important antigen-sampling cell to be investigated in order to devise novel methods to improve mucosal delivery of biologically active compounds. Recently, novel information on the interactions between bacteria and FAE have come to light that unveil further the complex cross-talk taking place at mucosal interfaces between bacteria, epithelial cells and the immune system and which are central to the formation and function of M cells. In particular, it has been shown that M cell mediated transport of antigen across the FAE is improved rapidly by exposure to certain bacteria, thus opening the way to identify new means to achieve a more effective mucosal delivery. Here, these novel findings and their potential in mucosal immunity are analysed and discussed, and new approaches to improve antigen delivery to the mucosal immune system are also proposed. [source] Hypercholesterolemia and inflammation in atherogenesis: Two sides of the same coinMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 11 2005Daniel SteinbergArticle first published online: 3 NOV 200 Abstract An abundance of experimental, clinical, and epidemiologic data capped by stunning interventional results with the statins has established hypercholesterolemia as a major causative factor in atherogenesis. In familial hypercholesterolemia and in animal models it is a sufficient cause. Some degree of hypercholesterolemia, perhaps 30,50 mg/dL, may even be a necessary cause. It is equally clear that from the very beginning atherogenesis has a strong inflammatory component, i. e., it is characterized by penetration of monocytes and of T-cells into the developing lesion. These cells, through the secretion of cytokines and growth factors, through immune responses, and through complex cross-talk with elements of the artery wall modulate the growth of the lesion and affect its stability. But inflammation has to occur in response to something. What is that something? What is the "injury" in "response-to-injury"? The case will be made that oxidized lipids in oxidized LDL or generated in response to prooxidative changes in the cells of the artery wall should be considered a plausible candidate. There is no need to consider hypercholesterolemia and inflammation as alternative hypotheses. Both are very much involved. Optimal intervention and prevention will probably require attention to both. [source] Layers of defense responses to Leptosphaeria maculans below the RLM1 - and camalexin-dependent resistancesNEW PHYTOLOGIST, Issue 2 2009Mattias Persson Summary ,,Plants have evolved different defense components to counteract pathogen attacks. The resistance locus resistance to Leptosphaeria maculans 1 (RLM1) is a key factor for Arabidopsis thaliana resistance to L. maculans. The present work aimed to reveal downstream defense responses regulated by RLM1. ,,Quantitative assessment of fungal colonization in the host was carried out using quantitative polymerase chain reaction (qPCR) and GUS expression analyses, to further characterize RLM1 resistance and the role of salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) in disease development. Additional assessments of A. thaliana mutants were performed to expand our understanding of this pathosystem. ,,Resistance responses such as lignification and the formation of vascular plugs were found to occur in an RLM1 -dependent manner, in contrast to the RLM1 -independent increase in reactive oxygen species at the stomata and hydathodes. Analyses of mutants defective in hormone signaling in the camalexin-free rlm1Lerpad3 background revealed a significant influence of JA and ET on symptom development and pathogen colonization. ,,The overall results indicate that the defense responses of primary importance induced by RLM1 are all associated with physical barriers, and that responses of secondary importance involve complex cross-talk among SA, JA and ET. Our observations further suggest that ET positively affects fungal colonization. [source] Dendritic cells in cytomegalovirus infection: viral evasion and host countermeasuresAPMIS, Issue 5-6 2009ALEXANDER RÖLLE Human cytomegalovirus (HCMV) is a ,-herpesvirus that infects the majority of the population during early childhood and thereafter establishes life-long latency. Primary infection as well as spontaneous reactivation usually remains asymptomatic in healthy hosts but can, in the context of systemic immunosuppression, result in substantial morbidity and mortality. HCMV counteracts the host immune response by interfering with the recognition of infected cells. A growing body of literature has also suggested that the virus evades the immune system by paralyzing the initiators of antiviral immune responses , the dendritic cells (DCs). In the current review, we discuss the effects of CMV (HCMV and murine CMV) on various DC subsets and the ensuing innate and adaptive immune responses. The impact of HCMV on DCs has mainly been investigated using monocyte-derived DCs, which are rendered functionally impaired by infection. In mouse models, DCs are targets of viral evasion as well, but the complex cross-talk between DCs and natural killer cells has, however, demonstrated an instrumental role for DCs in the control and clearance of viral infection. Fewer studies address the role of peripheral blood DC subsets, plasmacytoid DCs and CD11c+ myeloid DCs in the response against HCMV. These DCs, rather than being paralyzed by HCMV, are largely resistant to infection, mount a vigorous first-line defense and induce T-cell responses to the virus. This possibly provides a partial explanation for an intriguing conundrum: the highly efficient control of viral infection and reactivation in immunocompetent hosts in spite of multi-layered viral evasion mechanisms. [source] Regulation of bovine corneal endothelial cell cycle by transforming growth factor-,ACTA OPHTHALMOLOGICA, Issue 5 2003Yutaka Motegi Abstract. Purpose:,The transforming growth factor-, (TGF-,) family includes three multifunctional proteins, TGF-,1, TGF-,2 and TGF-,3, expressed in ocular tissue, which are involved in regulating cell differentiation, cell proliferation and other cell functions. TGF-, is present in aqueous humour and regulates corneal endothelial cells. This study explores the mechanism by which TGF-, regulates the cell cycle in cultured corneal endothelial cells. Methods:,The expression of specific receptors for the TGF-, family was investigated at the protein level by affinity cross-linking with radio-iodinated TGF-,1 and immunoprecipitation with specific antibodies to TGF-, receptors. Regulation of entry into the S-phase of the cell cycle was determined by 5-bromo-2, deoxyuridine (BrdU) incorporation into the cells. The signal transduction pathways were investigated using various blocking agents for protein kinase transducers involved in intracytoplasmic signal transduction. Results:,Cultured bovine corneal endothelial cells were confirmed to express TGF-, type 1 and type 2 receptors and endoglin. In the confluent state, TGF-,1 and TGF-,2 stimulated the cells to progress to the S-phase of the cell cycle through platelet-derived growth factor-B (PDGF-B) chain production and protein kinase C. Conclusions:,TGF-, accelerated cell cycle progression from the G0/G1 phase to the S-phase in cultured corneal endothelial cells, under our experimental conditions, through pathways involving protein kinase C. These pathways are related to the cross-talk between TGF-, and other cytokines. The conditions employed in the present experiments may be useful for investigating the complex cross-talk between various cytokines and growth factors. [source] | |||||||||||||