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Evidence for antigen presentation by human neutrophils

Evidence for antigen presentation by human neutrophils
Evidence for antigen presentation by human neutrophils
Neutrophils are the first migrating responders to sterile and infectious inflammation, and act in a powerful but non-specific fashion to kill a wide variety of pathogens. It is now clear that they can also act in a highly discriminating fashion; this is particularly evident in their interactions with other cells of the immune system. It is clear that neutrophils are present during the adaptive immune response, interacting with T cells in complex ways which differ between tissue types and disease state. One of the ways in which this interaction is mediated is by neutrophil expression of HLA molecules and presentation of antigen to T cells. In mice, this is well established to occur with both CD4+ and CD8+ T cells. However, the evidence is less strong with human cells. Here, we assembled available evidence for human neutrophil antigen presentation. We find that the human cells are clearly able to up-regulate HLA-DR and co-stimulatory molecules; are able to process protein antigen into fragments recognised by T cells; are able to enter lymph node T cell zones; and, in vitro, are able to present antigen to memory T cells, inducing proliferation and cytokine production. However, many questions remain, particularly concerning whether the cell-cell interactions can last for sufficient time to trigger naïve T cells. These experiments are now critical as we unravel the complex interactions between these cells and their importance for the development of human immunity.
0006-4971
2455-2463
Moffat, Angus
fbc72b8e-20d0-4999-b3dc-a644aa0e2047
Gwyer Findlay, Emily
b6787bbb-66ad-435c-ad2c-c18ffaf6b7d8
Moffat, Angus
fbc72b8e-20d0-4999-b3dc-a644aa0e2047
Gwyer Findlay, Emily
b6787bbb-66ad-435c-ad2c-c18ffaf6b7d8

Moffat, Angus and Gwyer Findlay, Emily (2024) Evidence for antigen presentation by human neutrophils. Blood, 143 (24), 2455-2463. (doi:10.1182/blood.2023023444).

Record type: Article

Abstract

Neutrophils are the first migrating responders to sterile and infectious inflammation, and act in a powerful but non-specific fashion to kill a wide variety of pathogens. It is now clear that they can also act in a highly discriminating fashion; this is particularly evident in their interactions with other cells of the immune system. It is clear that neutrophils are present during the adaptive immune response, interacting with T cells in complex ways which differ between tissue types and disease state. One of the ways in which this interaction is mediated is by neutrophil expression of HLA molecules and presentation of antigen to T cells. In mice, this is well established to occur with both CD4+ and CD8+ T cells. However, the evidence is less strong with human cells. Here, we assembled available evidence for human neutrophil antigen presentation. We find that the human cells are clearly able to up-regulate HLA-DR and co-stimulatory molecules; are able to process protein antigen into fragments recognised by T cells; are able to enter lymph node T cell zones; and, in vitro, are able to present antigen to memory T cells, inducing proliferation and cytokine production. However, many questions remain, particularly concerning whether the cell-cell interactions can last for sufficient time to trigger naïve T cells. These experiments are now critical as we unravel the complex interactions between these cells and their importance for the development of human immunity.

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Moffat Findlay 2024 revision 2 - Accepted Manuscript
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More information

Accepted/In Press date: 9 March 2024
e-pub ahead of print date: 20 March 2024
Published date: 20 March 2024

Identifiers

Local EPrints ID: 489241
URI: http://eprints.soton.ac.uk/id/eprint/489241
ISSN: 0006-4971
PURE UUID: db0414e0-bbdc-4ae7-8f11-e3a5524c91b7
ORCID for Emily Gwyer Findlay: ORCID iD orcid.org/0000-0002-2311-6589

Catalogue record

Date deposited: 18 Apr 2024 16:39
Last modified: 13 Jun 2024 02:04

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Contributors

Author: Angus Moffat
Author: Emily Gwyer Findlay ORCID iD

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