tetano
Editor, Senior Moderator
J Immunol. 2019 Jun 24. pii: ji1900093. doi: 10.4049/jimmunol.1900093. [Epub ahead of print]
[h=1]The Impact of TCR Signal Strength on Resident Memory T Cell Formation during Influenza Virus Infection.[/h] Fiege JK[SUP]1,[/SUP][SUP]2[/SUP], Stone IA[SUP]1,[/SUP][SUP]2[/SUP], Fay EJ[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Markman MW[SUP]1,[/SUP][SUP]2[/SUP], Wijeyesinghe S[SUP]1,[/SUP][SUP]2[/SUP], Macchietto MG[SUP]4[/SUP], Shen S[SUP]4[/SUP], Masopust D[SUP]1,[/SUP][SUP]2[/SUP], Langlois RA[SUP]5,[/SUP][SUP]2,[/SUP][SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Resident memory T cells (T[SUB]RM[/SUB]) in the lung are vital for heterologous protection against influenza A virus (IAV). Environmental factors are necessary to establish lung T[SUB]RM[/SUB]; however, the role of T cell-intrinsic factors like TCR signal strength have not been elucidated. In this study, we investigated the impact of TCR signal strength on the generation and maintenance of lung T[SUB]RM[/SUB] after IAV infection. We inserted high- and low-affinity OT-I epitopes into IAV and infected mice after transfer of OT-I T cells. We uncovered a bias in T[SUB]RM[/SUB] formation in the lung elicited by lower affinity TCR stimulation. TCR affinity did not impact the overall phenotype or long-term maintenance of lung T[SUB]RM[/SUB] Overall, these findings demonstrate that T[SUB]RM[/SUB] formation is negatively correlated with increased TCR signal strength. Lower affinity cells may have an advantage in forming T[SUB]RM[/SUB] to ensure diversity in the Ag-specific repertoire in tissues.
Copyright ? 2019 by The American Association of Immunologists, Inc.
PMID: 31235552 DOI: 10.4049/jimmunol.1900093
[h=1]The Impact of TCR Signal Strength on Resident Memory T Cell Formation during Influenza Virus Infection.[/h] Fiege JK[SUP]1,[/SUP][SUP]2[/SUP], Stone IA[SUP]1,[/SUP][SUP]2[/SUP], Fay EJ[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Markman MW[SUP]1,[/SUP][SUP]2[/SUP], Wijeyesinghe S[SUP]1,[/SUP][SUP]2[/SUP], Macchietto MG[SUP]4[/SUP], Shen S[SUP]4[/SUP], Masopust D[SUP]1,[/SUP][SUP]2[/SUP], Langlois RA[SUP]5,[/SUP][SUP]2,[/SUP][SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Resident memory T cells (T[SUB]RM[/SUB]) in the lung are vital for heterologous protection against influenza A virus (IAV). Environmental factors are necessary to establish lung T[SUB]RM[/SUB]; however, the role of T cell-intrinsic factors like TCR signal strength have not been elucidated. In this study, we investigated the impact of TCR signal strength on the generation and maintenance of lung T[SUB]RM[/SUB] after IAV infection. We inserted high- and low-affinity OT-I epitopes into IAV and infected mice after transfer of OT-I T cells. We uncovered a bias in T[SUB]RM[/SUB] formation in the lung elicited by lower affinity TCR stimulation. TCR affinity did not impact the overall phenotype or long-term maintenance of lung T[SUB]RM[/SUB] Overall, these findings demonstrate that T[SUB]RM[/SUB] formation is negatively correlated with increased TCR signal strength. Lower affinity cells may have an advantage in forming T[SUB]RM[/SUB] to ensure diversity in the Ag-specific repertoire in tissues.
Copyright ? 2019 by The American Association of Immunologists, Inc.
PMID: 31235552 DOI: 10.4049/jimmunol.1900093