We Hope you are enjoying the Hallway Art on the 5th floor.
We have started one floor at a time, hoping to refresh the division's appearance to the outside world! And to make our hallways fun to look at.
We plan to use some of the old glass frames to update info on the HPI division, as well as to showcase work from our labs.
For this reason, we ask that you submit any journal covers you may have scored and you are proud of over the years!
Submissions can be sent to: maria.hadjifrangiskou@vanderbilt.edu, helen.chomicki@vanderbilt.edu and/or tracy.bradford@vanderbilt.edu
HPI DIVISION ANNOUNCEMENTS
HPI division meeting: August 25, 2015 room A-5305 MCN, 3:00pm.
- Business meeting
August 14- 2nd Friday Happy Hour - Hosted by Algood and Cassat labs, room A5305 MCN, 4:00pm.
Funded! Our division has obtained a training grant, entitled "Chemical Biology of Infectious Diseases (CBID) Training Program" geared towards chemical biology approaches used to study infectious disease. Support for this year's recipients (Monique Bennett (Crowe lab), Aimee Wilde (Jim Cassat lab) and Maria Agostini (Mark Dennison lab)) is already underway. Congratulations to the first recipients!
Congratulations to Drs. Carrie Shaffer (Hadjifrangiskou Lab) and Joe Zackular (Skaar Lab); for successfully competing for post-doctoral NRSA funding.
Do not forget to send us your lab's successes if you want them featured!
Publications: A total of 20 new publications from HPI faculty have been posted on Pubmed in June. The listings and links to all publications follow below.
Hill T.M. et al, PLoS Pathogens 2015, Jun 11;11(6):e1004975
In this work from the Joyce lab, Hill et al. provide insights into the role of NKT cells in mediating the response to infection by the live vaccine strain of Francisella tularensis, in a mouse model of infection.
Type I, semi-invariant natural killer T (NKT) cells are innate-like lymphocytes with a demonstrated role in a wide range of diseases.
NKT cells express an invariant TCR α-chain (Vα14-Jα18 in mice and Vα24-Jα18 in humans) and one of a restricted set of TCR β-chains and, hence, called semi-invariant. Their name also reflects their hybrid nature, in that they co-express markers of both NK cells and conventional T cells.
Often cited for their ability to rapidly produce a variety of cytokines upon activation, NKT cells have long been appreciated for their ability to “jump-start” the immune system and to shape the quality of both the innate and adaptive response.
NKT cells are enriched within the lung vasculature where they are optimally positioned for early antigen encounter.
Hill et al., challenged mice intranasally with the live vaccine strain (LVS) of Francisella tularensis to probe the role of lung NKT cells in pulmonary tularemia. In pulmonary tularemia, patients typically show signs of systemic illness, which may be accompanied by immediate signs of respiratory disease and can result in death in 30–60% of cases if left untreated. Although the exact cause of death is unclear, it is likely due to an overwhelming systemic inflammatory response.
In their mouse models of infection, Hill and colleagues discovered that LVS infection activated iNKT cells which produced interferon (IFN)-γ and propagated a sepsis-like proinflammatory response that led to a lethal phenotype in wild type mice. This proinflammatory response was much tempered in CD1d-deficient mice that lacked NKT cells.
Strikingly, however, the mutant mice had increased lymphocytic infiltration in the lungs that organized into tertiary structures resembling induced bronchus-associated lymphoid tissue (iBALT) at the peak of infection.
iBALT are typically associated with chronic conditions and have been described in the lung for some viral infections.
Such early iBALT formation is suggestive of a more vigorous and effective adaptive immune response resulting in reduced systemic inflammation and therefore less severe disease. These findings suggest a suppressive/regulatory role for pulmonary NKT cells.
The regulatory function of NKT cells is just beginning to be elucidated and much of what we know derives from studies utilizing model antigens. The findings from the Joyce lab provide a model in which to study the potentially detrimental functions of iNKT cells in a natural infection.
What are your thoughts? Feel free to muse by sending us an email (maria.hadjifrangiskou@vanderbilt.edu, helen.chomicki@vanderbilt.edu)