Skip to main content

Main menu

  • Home
  • Articles
    • Current Issue
    • Next in The JI
    • Archive
    • Brief Reviews
      • Neuroimmunology: To Sense and Protect
    • Pillars of Immunology
    • Translating Immunology
    • Most Read
    • Top Downloads
    • Annual Meeting Abstracts
  • COVID-19/SARS/MERS Articles
  • Info
    • About the Journal
    • For Authors
    • Journal Policies
    • Influence Statement
    • For Advertisers
  • Editors
  • Submit
    • Submit a Manuscript
    • Instructions for Authors
    • Journal Policies
  • Subscribe
    • Journal Subscriptions
    • Email Alerts
    • RSS Feeds
    • ImmunoCasts
  • More
    • Most Read
    • Most Cited
    • ImmunoCasts
    • AAI Disclaimer
    • Feedback
    • Help
    • Accessibility Statement
  • Other Publications
    • American Association of Immunologists
    • ImmunoHorizons

User menu

  • Subscribe
  • Log in

Search

  • Advanced search
The Journal of Immunology
  • Other Publications
    • American Association of Immunologists
    • ImmunoHorizons
  • Subscribe
  • Log in
The Journal of Immunology

Advanced Search

  • Home
  • Articles
    • Current Issue
    • Next in The JI
    • Archive
    • Brief Reviews
    • Pillars of Immunology
    • Translating Immunology
    • Most Read
    • Top Downloads
    • Annual Meeting Abstracts
  • COVID-19/SARS/MERS Articles
  • Info
    • About the Journal
    • For Authors
    • Journal Policies
    • Influence Statement
    • For Advertisers
  • Editors
  • Submit
    • Submit a Manuscript
    • Instructions for Authors
    • Journal Policies
  • Subscribe
    • Journal Subscriptions
    • Email Alerts
    • RSS Feeds
    • ImmunoCasts
  • More
    • Most Read
    • Most Cited
    • ImmunoCasts
    • AAI Disclaimer
    • Feedback
    • Help
    • Accessibility Statement
  • Follow The Journal of Immunology on Twitter
  • Follow The Journal of Immunology on RSS

In This Issue

J Immunol April 1, 2019, 202 (7) 1909; DOI: https://doi.org/10.4049/jimmunol.1990003
  • Article
  • Figures & Data
  • Info & Metrics
  • PDF
Loading

Incompatibility Issues for NK Cells

Figure1
  • Download figure
  • Open in new tab
  • Download powerpoint

Allogeneic hematopoietic stem cell transplantation (HSCT) can be an effective treatment for hematologic malignancies but requires identification of HLA-haploidentical bone marrow donors. These transplants are also prone to causing graft-versus-host disease (GvHD) in recipients due to the presence of alloreactive donor T cells. In this issue, Willem et al. (p. 2141) examine how incompatibility of killer cell Ig-like receptors (KIR), which are expressed by NK cells and are specific to different HLA allotypes, influence clinical outcomes in HSCT patients who underwent T cell–replete HSCT. The authors observed a higher incidence of acute GvHD but decreased relapse in recipients with inhibitory KIR/HLA incompatibility, and that recovery of KIR2DL2/3+ and KIR3DL1+ NK cells 30 d posttransplant was inversely affected by KIR/HLA incompatibility. Patients who developed GvHD also had more NK cells with differentiated and activated phenotypes. These data suggest that KIR/HLA incompatibility can play a critical role in donor/recipient selection and transplant outcomes.

Factoring for Complement Control

The complement system is a critical part of innate immunity and uses several mechanisms to differentiate between self and nonself. The alternative pathway (AP) of complement activation is relatively indiscriminate and is engaged in constant surveillance of cell surfaces, but is tightly regulated by Factor H (FH) or the splice variant FH-like protein 1 (FHL-1). Dopler et al. (p. 2082) examined how FH and FHL-1 can regulate AP activity on self and nonself surfaces. They observed that FH had greater selectivity overall as it exhibits greater regulatory activity on self surfaces compared with FHL-1 and a greater regulatory penalty on nonself surfaces. FHL-1 was also shown to be rapidly cleared from plasma in mice and was detected at very low levels in human plasma. Together, these results provide deeper insights into how FH tightly controls AP activity in a manner that differs from FHL-1.

Increasing Yield and Function of Tissue-Resident Lymphocytes

Figure2
  • Download figure
  • Open in new tab
  • Download powerpoint

The release of NAD and ATP during tissue processing can lead to ARTC2.2-mediated ribosylation of P2RX7 in invariant NKT cells (iNKT) and CD8+ tissue-resident memory T cells (TRM). When P2RX7 is ribosylated by ARTC2.2, it leads to irreversible pore formation and ultimately, cell death. Borges da Silva et al. (p. 2153) have shown that processing tissue in the presence of antagonist nanoparticles against ARTC2.2 can increase the yield, viability, and function of tissue-resident iNKT and CD8+ TRM. The ex vivo recovery of iNKT and CD8+ TRM treated with anti-ARTC2.2 nanoparticles was significantly increased in nonlymphoid tissues. Additionally, treating animals with anti-ARTC2.2 nanoparticles prior to tissue recovery increased cell recovery and function of both iNKT and CD8+ TRM. Blockade of ARTC2.2 also promoted an increase in CD103− CD8+ TRM recovered from the small intestine, suggesting that these cells are more susceptible to P2RX7-mediated cell death and are underrepresented in traditional analysis. Taken together, these data show that significant cell death from the ARTC2.2/P2RX7 pathway may skew leukocyte analysis from tissue.

Macaque MAITs

Innate-like T cells found in the gut—MR1-restricted mucosal-associated invariant T (MAIT) cells—respond to bacterial and viral infections and have been shown to be depleted during HIV infection. MAIT cells have been characterized in humans but are not as well defined in nonhuman primate models. In this issue, Juno et al. (p. 2105) use a pigtail macaque (PTM) model to characterize MAIT cells before and during SIV/simian HIV (SHIV) infection. They develop a PTM-specific MR1 tetramer to track MAIT cells and observe many transcriptional and phenotypic similarities shared by human and PTM MAIT cells. Unlike human MAIT cells, PTM counterparts express low levels of the gut-homing integrin α4β7 in naive animals and show less enrichment in the gut and rectum. Acute SIV/SHIV infection induced proliferation and upregulation of α4β7 in PTM MAIT cells and recruitment to rectal mucosa. During chronic infection, peripheral PTM MAIT cells exhibit an activated phenotype, lack Tbet, and are not significantly depleted in mucosal tissues. These data indicate that differential expression of α4β7 in PTM and human MAIT cells impacts mucosal homing prior to infection and can influence proliferation and mucosal depletion during chronic infection.

  • Copyright © 2019 by The American Association of Immunologists, Inc.
PreviousNext
Back to top

In this issue

The Journal of Immunology: 202 (7)
The Journal of Immunology
Vol. 202, Issue 7
1 Apr 2019
  • Table of Contents
  • Table of Contents (PDF)
  • About the Cover
  • Advertising (PDF)
  • Back Matter (PDF)
  • Editorial Board (PDF)
  • Front Matter (PDF)
Print
Download PDF
Article Alerts
Sign In to Email Alerts with your Email Address
Email Article

Thank you for your interest in spreading the word about The Journal of Immunology.

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
In This Issue
(Your Name) has forwarded a page to you from The Journal of Immunology
(Your Name) thought you would like to see this page from the The Journal of Immunology web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
In This Issue
The Journal of Immunology April 1, 2019, 202 (7) 1909; DOI: 10.4049/jimmunol.1990003

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Share
In This Issue
The Journal of Immunology April 1, 2019, 202 (7) 1909; DOI: 10.4049/jimmunol.1990003
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like

Jump to section

  • Article
    • Incompatibility Issues for NK Cells
    • Factoring for Complement Control
    • Increasing Yield and Function of Tissue-Resident Lymphocytes
    • Macaque MAITs
  • Figures & Data
  • Info & Metrics
  • PDF

Related Articles

Cited By...

More in this TOC Section

  • Top Reads
  • In This Issue
  • In This Issue
Show more IN THIS ISSUE

Similar Articles

Navigate

  • Home
  • Current Issue
  • Next in The JI
  • Archive
  • Brief Reviews
  • Pillars of Immunology
  • Translating Immunology

For Authors

  • Submit a Manuscript
  • Instructions for Authors
  • About the Journal
  • Journal Policies
  • Editors

General Information

  • Advertisers
  • Subscribers
  • Rights and Permissions
  • Accessibility Statement
  • Public Access
  • Privacy Policy
  • Disclaimer

Journal Services

  • Email Alerts
  • RSS Feeds
  • ImmunoCasts
  • Twitter

Copyright © 2021 by The American Association of Immunologists, Inc.

Print ISSN 0022-1767        Online ISSN 1550-6606