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A variety of immune cell types contribute to disease in individuals with multiple sclerosis, an autoimmune condition of the central nervous system. Thomas Prod'homme and Scott Zamvil comment on the 'Bench to Bedside' approach, examining how recent basic research implicates the antigen-presenting cell in this disease. In our 'Bedside to Bench' column, Hans Link explores how recent clinical trials may bolster a mechanistic role for the B cell.
The energy-regulating hormone leptin affects signals emerging from certain brain regions. New results explore the nature of these signals, finding a central role for phosphoinositide-3 kinase in the brain and the endocannabinoid system in adipocytes (pages 667–675).
Clearance of platelets by the liver can help counteract the dangerous blood coagulation that can occur during sepsis. The mechanism involves clearance of platelets through the liver's Ashwell receptor, which binds to platelet glycoproteins altered by sepsis-causing bacteria (pages 648–655).
A variety of immune cell types contribute to disease in individuals with multiple sclerosis, an autoimmune condition of the central nervous system. Thomas Prod'homme and Scott Zamvil comment on the 'Bench to Bedside' approach, examining how recent basic research implicates the antigen-presenting cell in this disease. In our 'Bedside to Bench' column, Hans Link explores how recent clinical trials may bolster a mechanistic role for the B cell.
Kinase inhibitors such as imatinib (Gleevec) have improved the outlook for many people with chronic myeloid leukemia and related blood disorders. But such drugs do not target the leukemia stem cell population and may not be curative. Krause and Van Etten discuss several clinical studies that suggest that interferon-α may provide a solution by selectively eliminating leukemic stem cells—although only more basic research will tell us whether this is true and how it may happen.
Three postmortem studies examine long-term fetal transplants in subjects with advanced Parkinson's disease. The findings—such as the development of parkinsonian pathology in some transplanted neurons—underscore the limitations of this approach.
About 25% of the African-American population carries a gene variant that seems to protect against heart failure. The findings may have implications for the use of β-blockers (pages 510–517).
Allergens stimulate lymphocytes to become factories for secreted proteins that cause organ dysfunction in allergic diseases. Allergens are now shown to target dendritic cells, the cells responsible for processing and presenting antigens to T cells (pages 565–573).
The search is on for for vaccine adjuvants that boost the innate immune response and complement existing adjuvants. Mast cell activators may be one option (pages 536–541).
Three studies examine how resistance to chemotherapy develops in cancers deficient in BRCA1 and BRCA2. The mechanism involves restoration of BRCA1 and BRCA2 activity. Shah examines the implications for the clinic, such as the potential value of continuing treatment with cisplatin and similar agents even after drug resistance develops.
A strain of Escherichia coli that causes urinary tract infections seems to take hold in the body by interfering with signaling through Toll-like receptors (TLRs). The mechanism involves a secreted bacterial protein that is taken up by cells and clogs up the TLR signaling mechanism (pages 399–406).
Robo4 expression in emerging blood vessels can neutralize signaling through the angiogenic factor vascular endothelial growth factor (VEGF) and maintain vessel integrity. The findings could lead to new therapeutic targets for angiogenesis and vascular leakage (pages 448–453).
Only one drug is widely used to treat schistosomiasis, a chronic, neglected tropical disease caused by parasitic blood flukes. Fears of potential drug resistance have accelerated the search for new classes of antischistosome drugs. A promising candidate has now emerged (pages 407–412).
