Skip to main content

Immunology Update - May 2016

Welcome to our new regular monthly slot where we report on research from the world of immunology, highlighting work from BSI members that has hit the headlines over the past four weeks.

Differences in individuals’ immune responses linked to flu vaccine effectiveness

Swine flue virus

Scientists aiming to develop a method to predict who will and won’t respond optimally to the seasonal flu vaccine have identified key differences in individuals’ immune responses.

Researchers, led by Dr Gregory Poland and Dr Richard Kennedy from the Mayo Clinic, set out to examine how differences in an individual’s immune cells correlate to their response to the seasonal flu vaccine. They found that there was a significant difference in response to the flu vaccine between individuals.  People who had a better antibody response to the vaccine after 28 days had higher levels of HLA-DR (a cell surface protein which is a marker for immune stimulation) on a specialised type of dendritic cell.  Prior to vaccination, these people also had more B cells in their blood with more CD86 (a cell surface protein that allows the immune system to be activated quickly in response to a threat).

“Ultimately, we hope that increasing our understating of how the immune system functions at a cellular level will allow us to develop more effective vaccines,” commented Dr Poland.

Read the press release

Read the full article: Kennedy et al. 2016. Immunology doi: 10.1111/imm.12599

Do pathogens cause type 1 diabetes?

Pancreatic beta cells

Type 1 diabetes is an autoimmune condition where the insulin-producing beta cells of pancreas are destroyed, leading to the need for life-long insulin replacement.  Killer T-cells have previously been implicated as playing a major part in initiating this destruction of beta cells – however, it is as yet unclear what the triggers to this case of mistaken identity might be.  Now BSI members Dr David Cole and Professor Andy Sewell from Cardiff University have used the Diamond Light Source to shine powerful x-rays into isolated killer T-cells from a patient with type 1 diabetes to elucidate what makes these cells go rogue and destroy beta cells.

They found that these killer T-cells are highly ‘cross-reactive’, and respond to a variety of pathogen-derived antigens, which could lead to the breaking of self-tolerance and to the development of autoimmune disease, such as type 1 diabetes. Dr Cole commented, “We identified part of a bug that turns on killer T-cells so they latch onto beta cells. This finding sheds new light on how these killer T-cells are turned into rogues, leading to the development of type 1 diabetes.”

The team hope that this increase of our understanding into the mechanisms behind the development of type 1 diabetes will eventually lead to new ways to diagnose, prevent or treat type 1 diabetes.

Read the press release

Read the full article: Cole et al. 2016. Journal of Clinical Investigation 126 2191–2204. doi:10.1172/JCI85679.

The importance of resting phases in B cell development

B-lymphocyte cell

Researchers from the Babraham Institute have discovered a new mechanism used by B cells to rest up between developmental events.  B cells, which manufacture antibodies and are key players in our adaptive immune response, need to undergo several developmental stages before reaching maturity.

Writing in Science, the team found two RNA binding proteins, ZFP36L1 and ZFP36L2, are key in dictating the timings of these stages.  Both of these proteins were found to promote cell quiescence by blocking other RNA messages that instruct the cell to start dividing.  Mice without these proteins saw a 98% reduction in the number of mature B cells they possessed.

BSI member and senior author, Dr Martin Turner, said, “Our findings shed light on the intricate control and coordination of the cell cycle and show that these binding proteins probably form part of a common mechanism to regulate quiescence, not just one specific to developing B cells.”

Read the press release

Read the full article: Galloway et al. 2016. Science 352 453–459 doi:10.1126/science.aad5978

Image credits: Swine flu virus – (C) NIAID; Pancreatic beta cells – (C) Furcifer paradalis on Flickr via CC 2.0; B lymphocyte – (C) Blausen gallery 2014.Wikiversity Journal of Medicine. DOI:10.15347/wjm/2014.010. ISSN 20018762