When necessary, the lung slows down the immune system
HZI researchers explain the control of the T cell reaction in lung alveoli
The lung’s mucous membrane comes into contact daily with thousands of molecules – many of them are harmless and many are threatening. In the latter case, defence mechanisms need be activated. If defence overshoots the mark, then it has to be restricted. Moreover, the cells in the pulmonary alveoli, the so-called lung air sacs, can co-decide how the immune system should react. Scientists at the Helmholtz Centre for Infection Research (HZI) in Braunschweig have now discovered a communication channel between the pulmonary alveoli cells and the immune system’s defence cells, the T cells. The researches will publish their findings today in the “American Journal of Respiratory and Critical Care Medicine”, the leading journal in the field of lung diseases. “The regulatory effect of the lung cells on an immune reaction has been completely underestimated up until now”, states Dunja Bruder, Head of the “Immune Regulation” working group at the HZI. Now the researchers know how the epithelium cells in the lung reach the immune system.
“The cells in the lung’s mucous membrane are able to balance the immune reaction. They can work to aid or repress the inflammation, dependent on the messengers that they excrete”, says Marcus Gereke, a researcher in Dunja Bruder’s working group. For example, if the cells secrete TGF-beta, a messenger that represses inflammation, they are in the position to calm the immune system. Then regulatory T cells, so-called Tregs (reg. T cells) are allowed to develop there. These Tregs (reg. T cells) have the ability to attenuate the inflammatory reactions. This way the lung can be protected from an aggressive immune reaction that would endanger the respiratory function.
The mucous membrane cells can also increase inflammations by giving the signal to the pathogen defence. To this end, the mucous membrane cells appear on the fragmented surface of a pathogen, which can be identified by T cells. The T cells then connect to specific defence, through which inflammations in the lung’s mucous membrane can be elicited.
“For this reason, the mucous membrane cells are surprisingly an important part of the immune defence in the lung”, says Bruder. “These findings are important basic principles for the development of new, tailor-made therapies in the field of chronic lung diseases such as asthma and COPD, chronic obstructive pulmonary diseases. In the future the researchers want to try and identify further messengers that repress inflammation and to engage in more specific cell communication, in particular, to stimulate regulatory T cells and, in doing so, alleviate inflammatory reactions.
Title of the original publication:
Marcus Gereke, Steffen Jung, Jan Buer and Dunja Bruder: Alveolar Type II Epithelial Cells Present Antigen to CD4+ T Cells and Induce Foxp3+ Regulatory T Cells”; Am J Respir Crit Care Med Vol 179. pp 344–355, 2009