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Polyclonal lymphocyte activation and hypergammaglobulinemia characterize the acute phase of Chagas' disease, a debilitating condition caused by Trypanosoma cruzi. Such pathogenic hyper-reactivities not only compromise specific host defense against the pathogen, but may also contribute to infection-induced chronic autoimmune responses. Characterizing parasite-derived factors driving non-specific immune responses will provide insights for parasite evasion of host specific immunity. This study shows that T. cruzi trans-sialidase (TS) is one such polyclonal activator for normal murine lymphoid and non-lymphoid cells in at least three aspects. First, TS induces aggregation of immune cells and secretion of cytokines, such as IL-6. Second, TS is a T-independent B cell mitogen, directly stimulating polyclonal B cell proliferation independent of IL-6, CD40, CD43, Toll-like receptor-4 (TLR-4), and mIg crosslinking. While TS is mitogenic to wild-type B cells, mostly CD5- B2 cells, it fails to induce any proliferation of B cells from Bruton's tyrosine kinase (Btk)-defective X-linked immune deficient (xid) mice, suggesting that Btk is involved in TS signaling. Furthermore, in vivo administration of TS is followed by polyclonal Ig secretion that peaks 4-6 days after injection, before detectable TS-specific antibodies. Third, although TS does not directly stimulate T cells, it potentiates antigen specific and nonspecific T cell responses through the activation of APC, such as macrophages and B cells. TS potentiation is observed in splenocytes deficient of CD28, ICAM-1, CD40L or CD43. However, optimal TS-potentiation requires IL-6 and Btk, as it is significantly reduced in splenocytes from IL-6 -/- and xid mice. The C-terminal tandem repeat domain (LTR), but not the N-terminal catalytic domain (CD) of TS, is the active moiety that mediates TS-induced cell aggregation, IL-6 secretion, B cell and macrophage activation. At non-mitogenic concentrations, however, LTR inhibits mouse T cell activation and blocks TS-potentiated T cell response. A working model for the actions of TS, its domains and TS receptor is proposed. The results indicate that TS is a parasite-derived factor that directly and indirectly activates both APC and T cells, disturbing host lymphocyte homeostasis and cytokine regulation. Thus, TS may drive polyclonal lymphocyte activation in acute infection, potentially contributing to the immune evasion of the parasite, as well as the autoimmune abnormality in chronic Chagas' disease.
Chagas disease causes severe socioeconomic impact and a high medical cost in Latin America. WHO and the World Bank consider Chagas disease as the fourth most transmittable disease to have a major impact on public health in Latin America: 120 million persons are potentially exposed, 16 to 18 million of whom are presently infected, causing 45,000 to 50,000 deaths per year. It has been calculated that approximately 2.4 million potential working years are lost because of incapacity and mortality due to the disease, for an annual cost estimated at 20 billion Euros. American Trypanosomiasis provides a comprehensive overview of Chagas disease and discusses the latest discoveries concerning the three elements that compose the transmission chain of the disease: - The host: human and mammalian reservoirs - The insect vectors: domestic and sylvatic vectors - The causative parasite: Trypanosoma cruzi - Informs and updates on all the latest developments in the field - Contributions from leading authorities and industry experts
African trypanosomes are tsetse-transmitted protozoa that inhabit the extracellular compartment of host blood. They cause fatal sleeping sickness in people, and Nagana, a wasting and generally fatal disease, in cattle. While trypanosomes are most common to Africa (about 30% of Africa's cattle graze on the fringe of the tsetse habitat), some species have spread beyond its boarders to Asia, the Middle East and South America. The African Trypanosomes, volume one of World Class Parasites, is written for researchers, students and scholars who enjoy reading research that has a major impact on human health, or agricultural productivity, and against which we have no satisfactory defense. It is intended to supplement more formal texts that cover taxonomy, life cycles, morphology, vector distribution, symptoms and treatment. It integrates vector, pathogen and host biology and celebrates the diversity of approach that comprises modern parasitological research.
In the last decades, several in vitro and in vivo studies have revealed the existence of a very complex network between the neuroendocrine and immune system. Important molecular mechanisms underlying these interactions, in both physiological and pathological conditions, have also been described. Indeed, hormones play a pivotal role in the development and functional regulation of the immune system – both innate and acquired responses. Immune system cells present specific hormone receptors and themselves produce some hormones, thus influencing hormone secretion. More recently, the modulation of hormone secretion has been attempted for treating associated autoimmune disorders, further supporting the strong interplay between the endocrine and immune system. Distinguished experts, who have published extensively in their fields, have contributed comprehensive chapters to this volume. The focus is on the various aspects of endocrine-neuro-immune connections, providing an updated panorama - from basics to clinical applications - of current knowledge and still debated issues.
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The third component of complement, C3, is one of the most versatile proteins and an important participant in immune surveillance and immune response pathways. Its multifunctio nality is based on its ability to interact specifically with multiple serum complement proteins, cell surface receptors, and mem brant;-associated regulatory proteins. One of its most intriguing strategies of interaction with cell surfaces is the covalent binding of activated C3 through the internal thioester. The field has expanded over the past 10 years and a wealth of information has accumulated. C3 from various species and many of the human C3 binding proteins have been cloned and expressed. Numerous cellular responses mediated by the diffe rent fragments of C3 have been described. The findings that C3 interacts in a ligand-receptor-like fashion with proteins of nonself origin such as the gC of herpes simplex virus, a 70-kDa protein from Candida albicans, proteins from Epstein-Barr virus, etc. has opened a new field of investigation. The papers assembled in this volume summarize the wealth of data on the various aspects of the C3 interactions; together they bring to the reader new information on the chemistry, molecular gene tics, biology, and pathophysiology of C3 and C3-binding proteins. Emphasis is given to structural features as they relate to functions. Spring 1989 JOHN D. LAMBRIS, HANS J. MULLER-EBERHARD Table of Contents J. E. VOLANAKIS: Participation of C3 and Its Ligands in Complement Activation . . . . . . . . . . . 1 S. R. BARNUM, G. FEY, and B. F. TACK: Biosynthesis and Genetics of C3 . . . . . . . . . . . . .
Chagas' disease, which results from infection with the single cell parasite Trypanosoma cruzi, is a debilitating condition that is a major problem in many parts of Latin America. Rapid technical progress is now facilitating dissection of the molecular mechanisms of disease pathogenesis, a process that will ultimately provide new strategies to alleviate the enormous public health burden associated with the infection. In this book, international experts review the buoyant status of Chagas' disease research as we enter the "post-genome" era and speculate on how the new findings will impact on drug and vaccine development. The chapters outline how progress is being made on several fronts ranging from parasite population genetics to human immunology. Researchers, physicians and students with an interest in any aspect of molecular parasitology should find this book to be a valuable reference
Biological processes are driven by complex systems of functionally interacting signaling molecules. Thus, understanding signaling molecules is essential to explain normal or pathological biological phenomena. A large body of clinical and experimental data has been accumulated over these years, albeit in fragmented state. Hence, systems biological approaches concomitant with the understanding of each molecule are ideal to delineate signaling networks/pathways involved in the biologically important processes. The control of these signaling pathways will enrich our healthier life. Currently, there are more than 30,000 genes in human genome. However, not all the proteins encoded by these genes work equally in order to maintain homeostasis. Understanding the important signaling molecules as completely as possible will significantly improve our research-based teaching and scientific capabilities. This encyclopedia presents 350 biologically important signaling molecules and the content is built on the core concepts of their functions along with early findings written by some of the world’s foremost experts. The molecules are described by recognized leaders in each molecule. The interactions of these single molecules in signal transduction networks will also be explored. This encyclopedia marks a new era in overview of current cellular signaling molecules for the specialist and the interested non-specialist alike During past years, there were multiple databases to gather this information briefly and very partially. Amidst the excitement of these findings, one of the great scientific tasks of the coming century is to bring all the useful information into a place. Such an approach is arduous but at the end will infuse the lacunas and considerably be a streamline in the understanding of vibrant signaling networks. Based on this easy-approach, we can build up more complicated biological systems.