Different routes of bacterial infection induce long-lived TH1 memory cells and short-lived TH17 cells

 Pepper M, et al. Nature Immunology 11, 83-90 (2010)

Speaker: Alan Hsu (許翊輝)                                 Time: 14:10~15:00, Jun. 2, 2010

Commentator: Dr. Pei-Jane Tsai (蔡佩珍老師)    Place: Room 601

Abstract:

        It is well known that memory T cells play a crucial role in pathogen clearance and are mainly divided into central memory T cells (T_CM) and effector memory T cells (T_EM), but still unclear is do these memory T cells fit in any of the known profiles such as T_H1, T_H2, or T_H17 subsets in vivoas seen in vitro.

In this study by using tetramers of peptide and major histocompatibility complex II (pMHCII)  to sort out the effector and memory cells from the naïve cells and by previous immunization the authors observed in order to obtain the real memory cells. After immunizing the mice through intravenous or intranasal routes 24 days earlier they found that the memory T cell response was mostly IFN-γ and IL-17 respectfully. While these memory T cells resided in the spleen or lymph nodes with a half life of 40 days or so, and the amount in the bone marrow remained relatively constant. Interesting is the fact that the IL-17 producing memory cells were much less in number and were much short lived compared with the T_H1 or IFN-γ producing memory cells. The reason for the difference in cell number is majorly due to the original amount primed where intravenous infection route is primed in the spleen and intranasal routes in the lymph node where T cells are much less compared to the former. To address the issue of short life span in these T_H17 memory T cells, the authors looked into whether these cytokine producing were of T_CM or T_EM and finding that T_H1 memory cells were of T_EM profile while IL-17 producing cells were of a T_CM profile. And when measured for CD27 expression, knowing that that cells lacking CD27 were short lived. As expected these T_H17 memory T cells lacked the CD27 marker. Even transferring CD27^- T cells into a new host can’t rescue them from dying within 2 weeks at the same time discovering that these Cd27^- cells also lacked an apoptosis inhibitor Bcl-2. Furthermore these Cd27^- cells have weak homeostatic proliferation because the lack of IL-15R (CD122) while IL-15 works as a survival marker for the T cells, and if given a artificial agonist of CD122 proliferation will increase stating that it is indeed the underlying molecule.

References:

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