T cells become licensed in the lung to enter the central nervous system (Nature, 2012, 488:675-679)

報告日期: 2012/12/07
報告時間: 16:00/16:50
報告學生: 黃婉愉
講評老師: 凌斌
附件下載: 下載[1251-1349150079-1.pdf] 

T cells become licensed in the lung to enter the central nervous system

         Nature 2012 Aug 30; 488(7413):675-679

Speaker: Huang, Wan-Yu                                Date: 2012/12/07

Commentator: Dr. Ling, Pin                              Place: Room 602

In autoimmune disease, multiple sclerosis, how the immune cells enter the brain is of central importance to understanding the physiological and pathological processes of the central nervous system.

The research team from Gemeinnutzige-Hertie-Stittung and University Medical Center Gottingen describe a mechanism that allows disease inducing effector T cells to enter the brain. They use animal (Lewis rat) model of experimental autoimmune encephalopathy (EAE) to discover that disease-causing T cells (blast) cannot enter the brain immediately after activation. Instead, intravenously transferred T cell blasts gain the capacity to enter the CNS after residing transiently within the lung tissue. The transferred T cells move along and within the airways to bronchus-associated lymphoid tissue and lung draining mediastinal lymph nodes before they enter the blood circulation follow by entering the brain to cause the disease. During this period, T cells stop dividing and throttle their production of proteins that foment inflammation. Otherwise they are programmed for migration: they become more motile, and specialized receptors appear on their surface membranes. They also figure out the activated T cells creeping along the surface of the bronchial tubes but also crawling along the inner surface of airway, this may related to that human disease multiple sclerosis could be triggered by respiratory tract infection or lung irritants (eg. smoking). Moreover, recent studies use comprehensive genetic analysis identify various genes in persons suffering from multiple sclerosis, it is interesting , a significant number of these genes are the same as those in this study to be involved in the migratory programming of T cells.

 

References:

Swace, S. et al.  Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis. Nature 476, 214-219,2011

Bere, K et al.  Commensal microbiota and myelin autoantigen coopereate to trigger autoimmune demyelination.  Nature 479,538-541, 2011