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ABSTRACT
Introduction: The first mucosal site to encounter inhaled allergen, antigen, and microbes is the upper airway. It must perforce have a rapid system of environmental threat recognition and self-defense. B cells play a critical role in such airway host-defense, tissue surveillance, and immune modulation. Several common upper airway diseases can be defined in the expression of either exaggerated or dysregulated B-cell function within T2-high mucosal inflammatory states.
Areas covered: In this review, the authors discuss the immunology of allergic rhinitis (AR) and chronic rhinosinusitis with nasal polyps (CRSwNP) in the context of highlighting key aspects of B-cell biology and function. The review is based on the findings of a literature search using the terms B cells, rhinitis, nasal polyps, and rhinosinusitis.
Expert opinion: Despite the emerging role of B-cell overdrive and dysfunction in upper airway disease, studies are lacking specifics to B cells, particularly in association with sinonasal infection and mucosal inflammation. There is a pressing need to focus on how respiratory inflammation, alongside impaired or exaggerated B-cell function, amplifies and further dysregulates immune signaling pathways in the disease setting of AR and CRSwNP.
Abbreviations
| AICD | = | activation-induced cytidine deaminase |
| AR- | = | allergic rhinitis |
| APRIL- | = | a proliferation-inducing ligand |
| BAFF- | = | B cell activating factor |
| BCR- | = | B cell receptor |
| CRS- | = | chronic rhinosinusitis |
| CRSwNP- | = | chronic rhinosinusitis with nasal polyps |
| CRSsNP- | = | chronic rhinosinusitis without nasal polyps |
| CSR- | = | class switch recombination |
| DCs- | = | dendritic cells |
| EBV- | = | Epstein-Barr virus |
| fDC- | = | follicular dendritic cells |
| HDM- | = | house dust mite |
| ICAM- | = | 1-intercellular adhesion molecule-1 |
| ICOS- | = | inducible T-cell costimulatory |
| ICOSL - | = | inducible T-cell costimulatory ligand |
| Ig– | = | immunoglobulin |
| IL- | = | interleukin |
| ILCs- | = | innate lymphoid cells |
| LAR- | = | local allergic rhinitis |
| M cells- | = | microfold cells |
| MC- | = | mast cell |
| MIP- | = | macrophage inflammatory protein |
| NERD- | = | non-steroidal anti-inflammatory exacerbated respiratory disease |
| NF- | = | κB-nuclear factor κB |
| NP- | = | nasal polyp |
| pIgR- | = | polymeric immunoglobulin receptor |
| RANTES- | = | regulated on activation, normal T cell expressed and secreted |
| SAEs- | = | staphylococcus aureus enterotoxins |
| SLO- | = | secondary lymphoid organ |
| STAT- | = | signal transducer and activator of transcription proteins |
| TARC- | = | Thymus and activation regulated chemokine |
| TCR- | = | T cell receptor |
| TGF- | = | transforming growth factor |
| TfH - | = | T follicular helper |
| TSLP- | = | thymic stromal lymphopoietin |
| VCAM- | = | 1-vascular cell adhesion molecule 1 |
Acknowledgments
Figures drawn using Biorender.com.
Declaration of interest
Harsha H Kariyawasam (HHK) has undertaken paid consultancy work for Novartis and Sanofi and received lecture fees and support for conference attendance from GSK. He has undertaken paid lecture commitment for AstraZeneca. HHK has no other conflict of interest in relation to the topics covered in this review. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Article highlights
In allergic rhinitis and chronic rhinosinusitis with nasal polyps increasing evidence supports a significant B cell drive to disease. In the context of airway injury by allergen, antigen or microbes, B cells migrate into the airway mucosa. Clonal expansion, selection and cell differentiation into plasma cells all occur in the local airway mucosa, not just in secondary lymphoid organs. The upper airway mucosa is the predominant site for the development of IgE+ plasma cells.
B cells undergo somatic hypermutation and immunoglobulin class switching to generate multiple immunoglobulin isotypes, including excess IgE in the local sinonasal tissue.
B cells can now drive T2 inflammatory states, not just via functional antibody production but probably also through interactions with commensal microbes and other recruited inflammatory cells such as Th2 cells and eosinophils. This leads to immune amplification and dysregulation.
The exact fate of such local B cells in humans are uncertain but they may migrate back to the bone marrow to survive as long-lived IgE+ memory plasma cells that can re-populate sinonasal tissue effector cells with IgE, leading to disease activation.
Specific B cells directed therapies have not yet been considered for the treatment of upper airway disease.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.