The Role Of The Innate Immune Cells In The Development Of Type 1 Diabetes

Main Category: Diabetes
Also Included In: Immune System / Vaccines
Article Date: 31 Dec 2012 - 0:00 PST Current ratings for:
The Role Of The Innate Immune Cells In The Development Of Type 1 Diabetes

Julien Diana and Yannick Simoni of the "Immune Mechanisms in Type 1 Diabetes" (Inserm/Universite Paris Descartes), directed by Agnes Lehuen, have just published the results of their work on type 1 diabetes in the Nature Medicine journal. This is a disease characterised by the self-destruction of the p pancreatic cells that produce insulin. The researchers reveal the role of the innate immune cells, especially the dendritic cells, that cause the activation of the killer T-lymphocytes whose action is directed against the p pancreatic cells. The results obtained in mice make it possible to consider new ways of regulating the auto-immune reaction generated by the innate immune cells.

Type 1 diabetes, or insulin-dependent diabetes, is an auto-immune disease characterised by the destruction of insulin-producing pancreatic ß cells that are present in the Islets of Langerhans which are themselves in the pancreas. The peculiarity of this type of diabetes lies in the fact that the cells are destroyed by T lymphocytes that kill the patient's immune system. This is an auto-immune reaction. Much of the research has highlighted the role of auto-reactive T lymphocytes in the pancreatic ß cells. Yet the mechanisms involved in the initial activation of the immune system that triggers the sequence of events leading to the death of the cells are still ill-defined.

The work of the team working on "Immune mechanisms of Type 1 diabetes" (Inserm/Université de Paris Descartes) in NOD (Non-obese diabetic) mice, the model used for studying Type 1 diabetes, reveals the essential role played by the cells of the innate immune system[1] that were not hitherto considered to be involved in diabetes. These cells were known to play a role in other auto-immune diseases such as lupus and psoriasis. In this study, researchers managed to describe the mechanisms initiating the activation of T lymphocytes attaching themselves to the pancreatic ß cells.

The innate immune system is normally activated when an infection occurs. This is when the mobilisation and activation of neutrophils and dendritic cells is observed, constituting the first stages of the immune response. Abnormally in NOD diabetic mice, the natural physiological death of pancreatic ß cells, occurring as the process progresses, involves an innate auto-immune response in the pancreas. Researchers have provided details of the introduction of a sequence of activation events in these innate immune cells in the Islets of Langerhans.

The natural deterioration of the ß cells leaves cell debris in the tissues that abnormally activate the neutrophils. These alarm cells in the immune system warn the dendritic cells (pDC), which in turn cause the production of IFN a interferon, an alarm molecule. The interferon a then stimulates the T lymphocytes which, by recognising functional pancreatic ß cells, cause these cells to die.

"We have observed in mice that treatment prevents activation of the innate immune cells, neutrophils and dendritic cells, warning of the onset of diabetes by inhibiting the appearance of auto-immune T responses aimed at the pancreas" explains Agnès Lehuen, head of the Inserm team.

These results show, for the first time, the important role played by innate immune cells in the sequence of events leading to the onset of Type 1 diabetes. Researchers continue to strive to understand how to regulate the auto-immune reaction produced by dendritic cells without compromising the innate immune system, an essential one in cases of infection. Several routes are being taken to attempt to regulate the production of the INF a alarm molecule that precedes activation of the killer T-cells, for example, by specifically targeting certain activation routes for the pDC dendritic cells.

"These therapeutic approaches are currently being tested in other auto-immune diseases such as lupus and psoriasis. Such innovative treatments could be useful in the prevention of Type 1 diabetes. It will first be necessary, however, to perform studies in diabetic and pre-diabetic patients to be able to better understand how the innate immune cells function, something that has not been studied until recently in auto-immune diabetes," concludes Agnès Lehuen.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our diabetes section for the latest news on this subject. [1] System present from birth that makes it possible to initiate an immune response to infection, regardless of the infectious agent involved. It is distinguished from the “acquired” or so-called “adaptive” immune system that is a specific response involving recognition of the infectious agent and the memorising of the infectious event.

The research benefited from a grant from LabEx INFLAMEX as part of investment for the future and for the Ile-de-France region.

INSERM (Institut national de la santé et de la recherche médicale)

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New Insight Into How Schwann Cells Repair Damage To Peripheral Nervous System

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Main Category: Neurology / Neuroscience
Also Included In: Diabetes
Article Date: 04 Jun 2012 - 11:00 PDT Current ratings for:
'New Insight Into How Schwann Cells Repair Damage To Peripheral Nervous System'

Researchers have gained new insight into how cells that insulate the nerve cells in the peripheral nervous system, Schwann cells, protect and repair damage caused by disease and trauma.

The researchers state that their findings will help in the development of future treatments for the repair and improvement of damage to the peripheral nervous system.

The study, conducted by researchers from the Peninsula College of Medicine and Dentistry, University of Exeter, together with colleagues from Rutgers University, Newark, and University College London, is published in the journal Neuroscience.

The peripheral nervous system (PNS) consists of all the nerves outside of the brain and spinal cord. The main function of the PNS is to connect the central nervous system to the limbs and organs, thus allowing us to feel the sun on our face and motor information, that allows us to move.

However, the PNS can be damaged through trauma and can occur in individuals with common inherited conditions, such as Charcot-Marie-Tooth (CMT) disease, and in diabetic neuropathy - which almost half of individuals with diabetes suffer from.

Symptoms include: Losing sensation in the hands and feetBladder control problemsDigestion problemsSexual function problemsProblems with blood pressure regulation Schwann cells provide the myelin sheath (insulation) for the nerve cells that transmit electrical signals to and form the spinal cord. The Schwann cells are able to transform back to an immature 'repair' cell due to their plasticity, thus allowing them to repair damage to the PNS. Although these cells are able to repair damage well, incomplete repair, perhaps after the severance of a nerve, may result in pain and long-term loss of function.

Although these cells are able to demyelinate, this makes them vulnerable to diseases, such as CMT, which affects 1 in 2,500 people. Variations in different CMT genes can cause cycles of repair and re-insulation (re-myelination). This can cause both Schwann cells and nerve cells to die as well as long-term damage. At present, there is no treatment for CMT and those with the disease suffer from increased sensory and motor problems which could leave them permanently disabled.

According to the researchers, findings from this study will lead to therapies to improve damage from severe trauma and stop the damage caused by CMT. Furthermore, they note that their may be the potential to improve repair in cases of diabetic neuropathy.

Professor David Parkinson, Associate Professor in Neuroscience, Peninsula College of Medicine and Dentistry, University of Exeter, explained:

"The findings of our research are excited because we have pinpointed and are understanding the mechanism by which our bodies can repair damage to the peripheral nervous system. With further investigation, this could well lead to therapies to repair nerve damage from trauma and mitigate the damage which related to common illnesses, such as CMT."

Written By Grace Rattue
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our neurology / neuroscience section for the latest news on this subject. p38 MAPK Activation Promotes Denervated Schwann Cell Phenotype and Functions as a Negative Regulator of Schwann Cell Differentiation and Myelination
David P. Yang, Jihyun Kim, Neeraja Syed, Young-john Tung, Ambily Bhaskaran, Thomas Mindos, Rhona Mirsky, Kristjan R. Jessen, Patrice Maurel, David B. Parkinson, and Haesun A. Kim
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Adult Stem Cells From Bone Marrow

Main Category: Stem Cell Research
Also Included In: Diabetes;  Parkinson's Disease;  Alzheimer's / Dementia
Article Date: 05 Jul 2012 - 1:00 PDT Current ratings for:
Adult Stem Cells From Bone Marrow

Researchers from the University of Maryland School of Maryland report promising results from using adult stem cells from bone marrow in mice to help create tissue cells of other organs, such as the heart, brain and pancreas - a scientific step they hope may lead to potential new ways to replace cells lost in diseases such as diabetes, Parkinson's or Alzheimer's. The research in collaboration with the University of Paris Descartes is published online in Comptes Rendus Biologies, a publication of the French Academy of Sciences.

"Finding stem cells capable of restoring function to different damaged organs would be the Holy Grail of tissue engineering," says lead author David Trisler, PhD, assistant professor of neurology at the University of Maryland School of Medicine.

He adds, "This research takes us another step in that process by identifying the potential of these adult bone marrow cells, or a subset of them known as CD34+ bone marrow cells, to be 'multipotent,' meaning they could transform and function as the normal cells in several different organs."

University of Maryland researchers previously developed a special culturing system to collect a select sample of these adult stem cells in bone marrow, which normally makes red and white blood cells and immune cells. In this project, the team followed a widely recognized study model, used to prove the multipotency of embryonic stem cells, to prove that these bone marrow stem cells could make more than just blood cells. The investigators also found that the CD34+ cells had a limited lifespan and did not produce teratomas, tumors that sometimes form with the use of embryonic stem cells and adult stem cells cultivated from other methods that require some genetic manipulation.

"When taken at an early stage, we found that the CD34+ cells exhibited similar multipotent capabilities as embryonic stem cells, which have been shown to be the most flexible and versatile. Because these CD34+ cells already exist in normal bone marrow, they offer a vast source for potential cell replacement therapy, particularly because they come from a person's own body, eliminating the need to suppress the immune system, which is sometimes required when using adults stem cells derived from other sources," explains Paul Fishman, MD, PhD, professor of neurology at the University of Maryland School of Medicine.

The researchers say that proving the potential of these adult bone marrow stem cells opens new possibilities for scientific exploration, but that more research will be needed to see how this science can be translated to humans.

"The results of this international collaboration show the important role that University of Maryland School of Medicine researchers play in advancing scientific understanding, investigating new avenues for the development of potentially life-changing treatments," says E. Albert Reece, M.D., Ph.D., M.B.A., vice president for medical affairs at the University of Maryland and the John Z. and Akiko K. Bowers Distinguished Professor and dean of the University of Maryland School of Medicine.

This project builds on three decades of collaboration between the American and French researchers, particularly Dr. Bernard Pessac of the University of Paris Descartes and Dr. Trisler at the University of Maryland. Researchers from the Multiple Sclerosis Center of Excellence at the Baltimore Veterans Administration Medical Center also contributed to the study.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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