The Myeloid-T Lymphocyte Axis in Chronic Lung Allograft Rejection: Emerging Insights into the Immune Circuitry Driving Fibrosis.

Sajad Moshkelgosha, Sumiha Ramendra, Ke Fan Bei, Stephen Juvet

Abstract readReview

In one paragraph

Review in Results and problems in cell differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing papers in PubMed

–field-weighted citation impact

1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Sajad Moshkelgosha *Latner Thoracic Research Laboratories, Toronto General Hospital Research Institute, University Health Network, Toronto, ON, Canada.

Sumiha Ramendra *Latner Thoracic Research Laboratories, Toronto General Hospital Research Institute, University Health Network, Toronto, ON, Canada.

Ke Fan BeiLatner Thoracic Research Laboratories, Toronto General Hospital Research Institute, University Health Network, Toronto, ON, Canada.

Stephen JuvetLatner Thoracic Research Laboratories, Toronto General Hospital Research Institute, University Health Network, Toronto, ON, Canada. stephen.juvet@uhn.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While lung transplantation is a life-saving treatment option for patients with end-stage lung diseases, its long-term outcome is hampered by exceedingly high rates of chronic rejection, manifesting as chronic lung allograft dysfunction (CLAD). It has long been recognized that exposure of the lung to the external environment via the airways, coupled with its rich immune microenvironment, makes the lung uniquely susceptible to heightened alloimmunity. Extensive immunosuppressive drugs do not provide effective control of the process of chronic rejection, and so, in recent years, investigators have turned their attention toward the identification of underlying cellular mechanisms that are either inherently resistant to or evolve to escape these medications. In this review, we explore recent advances in identifying the cellular mediators of chronic lung allograft rejection, with a focus on the myeloid-T cell immune axis, which will require targeted therapeutic approaches in the future to prevent irreversible allograft fibrosis.

Indexed as

Graft RejectionLung TransplantationMyeloid CellsT-LymphocytesAllograftsAnimalsChronic DiseaseFibrosisHumansChronic lung allograft dysfunctionInnate immunityLung transplantationMyeloid cellsTertiary lymphoid organsTissue resident memory T cells

Identifiers

PMID41479027

DOI10.1111/j.1600-6143.2004.00505.x

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