Posts Tagged Lymphoma

Discovery of new white blood cell reveals target for better vaccine design


ScienceDaily (July 27, 2012) — Researchers in Newcastle and Singapore have identified a new type of white blood cell which activates a killing immune response to an external source — providing a new potential target for vaccines for conditions such as cancer or Hepatitis B.

Publishing in the journal Immunity, the team of researchers from Newcastle University in collaboration with A*STAR’s Singapore Immunology Network (SIgN) describe a new human tissue dendritic cell with cross-presenting function.

Dendritic cells (DCs) are a type of white blood cell that orchestrate our body’s immune responses to infectious agents such as bacteria and viruses, as well as cancer cells. They are also very important for eliciting the immune response generated by vaccines.

DCs kick start an immune response by presenting small fragments of molecules from micro-organisms such as bacteria and viruses, or from vaccines or tumours, called antigens on their surface. This leads to activation of another white blood cell subset called T cells, which specialise in killing cells and are crucial for eliminating cancerous or infected cells. Most cells are only able to present antigens from within themselves, and so will only elicit an immune response if they are infected themselves. Only a specialised subset of DCs is able to generate a response to an external source of antigen, for example bacteria, vaccines and tumours.

The identity of human tissue DCs that are capable of presenting external antigen to activate the cell-killing response by T cells — a process termed ‘cross-presentation’ — has remained a mystery. Their discovery, as revealed by this research, will help scientists to design better targeted vaccine strategies to treat cancer and infections such as Hepatitis B.

“These are the cells we need to be targeting for anti-cancer vaccines,” said Dr Muzlifah Haniffa, a Wellcome Trust Intermediate Fellow and Senior Clinical Lecturer at Newcastle University. “Our discovery offers an accessible, easily targetable system which makes the most of the natural ability of the cell.” The researchers also showed for the first time that dendritic cell subsets are conserved between species and have in effect created a map, facilitating the translation of mouse studies to the human immune system.

“The cross-species map is in effect a Rosetta stone that deciphers the language of mouse into human,” explains Matthew Collin, Professor of Haematology from Newcastle University.

In the paper the researchers describe how the cross-presenting DCs were first isolated from surplus plastic surgery skin which was digested to melt the gelatinous collagen to isolate the cells. This research will have significant impact on the design of vaccines and other targeted immunotherapies.

The Rosetta Stone of our immune system: Mapping Human and Mouse dendritic cells

The Newcastle University team in collaboration with A*STAR’s Singapore Immunology Network (SIgN) have for the first time ever aligned the dendritic cell subsets between mouse and humans allowing the accurate translation of mouse studies into the human model for the first time.

The researchers isolated the dendritic cells from human blood and skin and those from mouse blood, lung and liver. Using gene expression analysis, they identified gene signatures for each human dendritic cell subset. Mouse orthologues of these genes were identified and a computational analysis was performed to match subsets across species.

This provides scientists for the first time with an accurate model to compare DCs between species. Professor Matthew Collin explains: “This is in effect a Rosetta stone that deciphers the language of mouse into human. It can put into context the findings from the extensive literature using mouse models to the human settings.”

Dr. Haniffa added: “These gene signatures are available in a public repository accessible for all researchers to benefit from the data. It will allow detailed knowledge of individual human dendritic cell subsets to enable specific targeting of these cells for therapeutic strategy.”

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The above story is reprinted from materials provided by Newcastle University.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Muzlifah Haniffa, Amanda Shin, Venetia Bigley, Naomi McGovern, Pearline Teo, Peter See, Pavandip Singh Wasan, Xiao-Nong Wang, Frano Malinarich, Benoit Malleret, Anis Larbi, Pearlie Tan, Helen Zhao, Michael Poidinger, Sarah Pagan, Sharon Cookson, Rachel Dickinson, Ian Dimmick, Ruth F. Jarrett, Laurent Renia, John Tam, Colin Song, John Connolly, Jerry K.Y. Chan, Adam Gehring, Antonio Bertoletti, Matthew Collin, Florent Ginhoux. Human Tissues Contain CD141hi Cross-Presenting Dendritic Cells with Functional Homology to Mouse CD103 Nonlymphoid Dendritic Cells. Immunity, 2012; 37 (1): 60 DOI: 10.1016/j.immuni.2012.04.012

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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Tumor cells’ inner workings predict cancer progression


ScienceDaily (July 27, 2012) — Using a new assay method to study tumor cells, researchers at the University of California, San Diego School of Medicine and UC San Diego Moores Cancer Center have found evidence of clonal evolution in chronic lymphocytic leukemia (CLL). The assay method distinguishes features of leukemia cells that indicate whether the disease will be aggressive or slow-moving, a key factor in when and how patients are treated.

The findings are published in the July 26, 2012 First Edition online issue of Blood.

The progression of CLL is highly variable, dependent upon the rate and effects of accumulating monoclonal B cells in the blood, marrow, and lymphoid tissues. Some patients are symptom-free for years and do not require treatment, which involves the use of drugs that can cause significant side effects and are not curative. In other patients, however, CLL is relatively aggressive and demands therapeutic intervention soon after diagnosis.

“Our study shows that there may not be a sharp dividing line between the more aggressive and less aggressive forms of CLL,” said Thomas J. Kipps, MD, PhD, Evelyn and Edwin Tasch Chair in Cancer Research and senior author of the study. “Instead, it seems that over time the leukemia cells of patients with indolent disease begin to use genes similar to those that are generally used by CLL cells of patients with aggressive disease. In other words, prior to requiring therapy, the patterns of genes expressed by CLL cells appear to converge, regardless of whether or not the patient had aggressive versus indolent disease at diagnosis.”

Existing markers for aggressive or indolent disease are mostly fixed and have declining predictive value the longer the patient is from his or her initial diagnosis. When the blood sample is collected, these markers cannot reliably predict whether a CLL patient will need therapy soon, particularly when the patient has had the diagnosis of CLL for many years.

Kipps and colleagues studied thousands of genes, particularly those that code for proteins, in a group of 130 CLL patients with varying risks of disease progression. They identified 38 prognostic subnetworks of interacting genes and proteins that, at the time of sample collection, indicate the relative the aggressiveness of the disease and predict when the patient will require therapy. They confirmed their work using the method on two other, smaller CLL patient cohorts in Germany and Italy.

The subnetworks offer greater predictive value because they are based not on expression levels of individual genes or proteins, but on how they dynamically interact and change over time, influencing the course of the CLL and patient symptoms.

“In a sense, we looked at families rather than individuals,” said Kipps. “If you find in an interconnected family where most genes or proteins are expressed at higher levels, it becomes more likely that these genes and proteins have functional significance.”

He added that while the subnetworks abound in data, their complexity actually makes them easy to interpret and understand. “It’s like when you look out of a window and see the sky, clouds, trees, people, cars. You’re getting tremendous amounts of information that individually doesn’t tell you much. But when you look at the scene as a whole, you see patterns and networks. This work is similar. We’re taking all of the individual gene expression patterns and making sense of them as a whole. We’re more able to more clearly see how they control and regulate function.”

The findings help define how CLL — and perhaps other cancers — evolve over time, becoming more aggressive and deadly. “It’s as if each tumor has a clock which determines how frequently it may acquire the chance changes that make it behave more aggressively. Although the rates can vary, it appears that tumors march down similar pathways, which converge over time to a point where they become aggressive enough to require therapy.”

The study may alter how scientists think about CLL and how clinicians treat the disease: whether it is better to wait for later stages of the disease when tumor cells are more fragile and easier to kill, or treat early-stage indolent tumor cells aggressively, when they are fewer in number but harder to find and more resistant to therapy.

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Story Source:

The above story is reprinted from materials provided by University of California – San Diego, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Han-Yu Chuang, Laura Rassenti, Michelle Salcedo, Kate Licon, Alexander Kohlmann, Torsten Haferlach, Robin Foà, Trey Ideker, and Thomas J. Kipps. Subnetwork-based analysis of chronic lymphocytic leukemia identifies pathways that associate with disease progression. Blood, July 26, 2012 DOI: 10.1182/blood-2012-03-416461

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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