Immune mechanisms in fibrotic interstitial lung disease

被引：9

作者：

Kamiya, Mari ^{[1
,2
]}

Carter, Hannah ^{[3
]}

Espindola, Milena S. ^{[4
]}

Doyle, Tracy J. ^{[1
,2
]}

Lee, Joyce S. ^{[5
]}

Merriam, Louis T. ^{[1
]}

Zhang, Fan ^{[6
,7
]}

Kawano-Dourado, Leticia ^{[8
,9
]}

Sparks, Jeffrey A. ^{[2
,10
]}

Hogaboam, Cory M. ^{[4
]}

Moore, Bethany B. ^{[3
]}

Oldham, William M. ^{[1
,2
]}

Kim, Edy Y. ^{[1
,2
]}

机构：

[1] Brigham & Womens Hosp, Dept Med, Div Pulm & Crit Care Med, Boston, MA 02115 USA

[2] Harvard Med Sch, Boston, MA 02115 USA

[3] Univ Michigan, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA

[4] Cedars Sinai Med Ctr, Dept Med, Div Pulm & Crit Med, Los Angeles, CA 90048 USA

[5] Univ Colorado, Sch Med, Dept Med, Aurora, CO 80045 USA

[6] Univ Colorado, Sch Med, Dept Med, Div Rheumatol, Aurora, CO 80045 USA

[7] Univ Colorado, Sch Med, Dept Biomed Informat, Aurora, CO 80045 USA

[8] Hcor Hosp, Hcor Res Inst, BR-04004030 Sao Paulo, SP, Brazil

[9] Univ Sao Paulo, Heart Inst InCor, Pulm Div, BR-05403900 Sao Paulo, SP, Brazil

[10] Brigham & Womens Hosp, Dept Med, Div Rheumatol Inflammat & Immun, Boston, MA 02115 USA

来源：

CELL | 2024年 / 187卷 / 14期

基金：

美国国家卫生研究院; 新加坡国家研究基金会;

关键词：

IDIOPATHIC PULMONARY-FIBROSIS; COLONY-STIMULATING FACTOR; B-CELL DIFFERENTIATION; SYSTEMIC-SCLEROSIS; NEUTROPHIL ELASTASE; HYPERSENSITIVITY PNEUMONITIS; GENETIC SUSCEPTIBILITY; COMPLEMENT ACTIVATION; LIGAND INTERACTIONS; ANIMAL-MODELS;

D O I：

10.1016/j.cell.2024.05.015

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Fibrotic interstitial lung diseases (fILDs) have poor survival rates and lack effective therapies. Despite evidence for immune mechanisms in lung fibrosis, immunotherapies have been unsuccessful for major types of fILD. Here, we review immunological mechanisms in lung fibrosis that have the potential to impact clinical practice. We first examine innate immunity, which is broadly involved across fILD subtypes. We illustrate how innate immunity in fILD involves a complex interplay of multiple cell subpopulations and molecular pathways. We then review the growing evidence for adaptive immunity in lung fibrosis to provoke a re-examination of its role in clinical fILD. We close with future directions to address key knowledge gaps in fILD pathobiology: (1) longitudinal studies emphasizing early-stage clinical disease, (2) immune mechanisms of acute exacerbations, and (3) next-generation immunophenotyping integrating spatial, genetic, and single-cell approaches. Advances in these areas are essential for the future of precision medicine and immunotherapy in fILD.

引用

页码：3506 / 3530

页数：25

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