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Nasal-associated lymphoid tissues (NALTs) support the recall but not priming of influenza virus-specific cytotoxic T cells

tetano

Editor, Senior Moderator
Proc Natl Acad Sci U S A. 2017 May 1. pii: 201620194. doi: 10.1073/pnas.1620194114. [Epub ahead of print]
[h=1]Nasal-associated lymphoid tissues (NALTs) support the recall but not priming of influenza virus-specific cytotoxic T cells.[/h] Pizzolla A[SUP]1[/SUP], Wang Z[SUP]1[/SUP], Groom JR[SUP]2[/SUP], Kedzierska K[SUP]1[/SUP], Brooks AG[SUP]1[/SUP], Reading PC[SUP]1,[/SUP][SUP]3[/SUP], Wakim LM[SUP]4[/SUP].
[h=3]Author information[/h]

[h=3]Abstract[/h] The lymphoid tissue that drains the upper respiratory tract represents an important induction site for cytotoxic T lymphocyte (CTL) immunity to airborne pathogens and intranasal vaccines. Here, we investigated the role of the nasal-associated lymphoid tissues (NALTs), which are mucosal-associated lymphoid organs embedded in the submucosa of the nasal passage, in the initial priming and recall expansion of CD8[SUP]+[/SUP] T cells following an upper respiratory tract infection with a pathogenic influenza virus and immunization with a live attenuated influenza virus vaccine. Whereas NALTs served as the induction site for the recall expansion of memory CD8[SUP]+[/SUP] T cells following influenza virus infection or vaccination, they failed to support activation of na?ve CD8[SUP]+[/SUP] T cells. Strikingly, NALTs, unlike other lymphoid tissues, were not routinely surveyed during the steady state by circulating T cells. The selective recruitment of memory T cells into these lymphoid structures occurred in response to infection-induced elevation of the chemokine CXCL10, which attracted CXCR3[SUP]+[/SUP] memory CD8[SUP]+[/SUP] T cells. These results have significant implications for intranasal vaccines, which deliver antigen to mucosal-associated lymphoid tissue and aim to elicit protective CTL-mediated immunity.


[h=4]KEYWORDS:[/h] CD8 T-cell priming; influenza virus; nasal-associated lymphoid tissue; respiratory tract

PMID: 28461487 DOI: 10.1073/pnas.1620194114
 
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