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Am. J. Respir. Crit. Care Med. · Mar 2019
Increased IgA Expression in Lung Lymphoid Follicles in Severe COPD.
- Maha Zohra Ladjemi, Clémence Martin, Marylène Lecocq, Bruno Detry, NanaFrank AboubakarFA1 Pôle de Pneumologie, ORL & Dermatologie., Charlotte Moulin, Birgit Weynand, Chantal Fregimilicka, Caroline Bouzin, Pascal Thurion, François Carlier, Jef Serré, Ghislaine Gayan-Ramirez, Monique Delos, Sebahat Ocak, Pierre Régis Burgel, and Charles Pilette.
- 1 Pôle de Pneumologie, ORL & Dermatologie.
- Am. J. Respir. Crit. Care Med. 2019 Mar 1; 199 (5): 592602592-602.
RationaleAccumulation of B cells and lymphoid follicles (LFs) has been described in chronic obstructive pulmonary disease (COPD) airways, but the functional status of lung B cells remains poorly known.ObjectivesTo characterize LFs for expression of IgA, the main mucosal antibody.MethodsThe presence of B cells and LFs, including intrafollicular IgA expression, were determined in the lung from patients with COPD (n = 37) versus control subjects (n = 34) by immunohistochemistry. We also evaluated follicular IgA responses in the lungs from mice infected with Pseudomonas aeruginosa (PAO1) (n = 10 per group) and in smoking mice.Measurements And Main ResultsWhereas in smokers B-cell numbers slightly increased, robust increases in B-cell and LF numbers (mainly in distal airways) were only observed in severe COPD. Most follicular B cells were IgM+ (70-80%), but IgA+ (and not IgG+) B-cell numbers were increased in LFs from severe COPD compared with control subjects (twofold, 44.7% vs. 25.2%), and this was significant in distal but not proximal airways. Follicular IgA response was also observed in PAO1-infected mouse lungs, but not after smoke exposure. Moreover, follicular IgA expression associated with expression of IL-21, which was very potent to activate immunoglobulin production in vitro.ConclusionsThis study shows that IgA production occurs in peribronchiolar LFs from severe COPD, where IL-21-producing T cells are present, and presumably represents a feature of exacerbated mucosal adaptive immune responses against microbial and/or self-antigens.
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