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Type 2 Inflammation in Upper and Lower Airway Diseases
Type 2 Inflammation in Upper and Lower Airway Diseases
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Type 2 Inflammation

Declaration of sponsorship Sanofi and Regeneron
Last updated:11th May 2022
Published:11th May 2022

What is Type 2 Inflammation?

Type 2 inflammation is a common driver for underlying pathophysiology across multiple inflammatory diseases, including asthma and chronic rhinosinusitis with nasal polyps (CRSwNP)1

Involving both the adaptive and innate arms of the immune system, type 2 inflammation is characterized by key cytokines, particularly interleukin (IL)-4, IL-13, and IL-5 (FIGURE 1).1,2​


FIGURE 1: Type 2 Inflammation Is Driven by Both the Adaptive and Innate Arms of the Immune System.1,3-8 *Downstream from Th2 cells, innate cells (such as mast cells and basophils) can also play a role in adaptive immunity given their activation by antigen-bound IgE. Crosslinking of IgE on these cells leads to release of several inflammatory mediators (including IL-4 and IL-13), thus amplifying the type 2 inflammatory response.1 IgE, immunoglobulin E; ILC2, type 2 innate lymphoid cell; Th2, T helper type 2.

Underlying type 2 inflammation plays a role across multiple diseases in a range of organ systems (FIGURE 2).1,9-18


FIGURE 2: Type 2 Inflammation Plays a Role Across Multiple Diseases.1,9-18 AERD, aspirin-exacerbated respiratory disease; COPD, chronic obstructive pulmonary disease; NSAID-ERD, non-steroidal anti-inflammatory drug-exacerbated respiratory disease.

Burden of Disease

Type 2 inflammatory diseases, including asthma and CRSwNP, are associated with substantial disease-specific signs, symptoms, and impaired quality of life (FIGURE 3).14,19-21


FIGURE 3: Common Aspects of Diseases Mediated by Type 2 Inflammation.14,19-21


Multiple type 2 inflammatory diseases such as asthma, CRSwNP, atopic dermatitis, and eosinophilic esophagitis have a common underlying pathophysiology.1

Type 2 Inflammation: Pathophysiologic Features That Underlie Multiple Inflammatory Diseases

Watch this short video to learn about the common pathophysiology underlying type 2 inflammatory diseases, including asthma and CRSwNP. Clinical manifestations from this shared pathophysiology and the additional burden from coexisting type 2 inflammatory diseases are also presented, supporting the key and central role of IL-4 and IL-13 in type 2 inflammation across multiple diseases.

Unifying the Heterogeneous Pathophysiology of Type 2 Inflammatory Diseases

Hear Prof. Oscar Palomares discuss the latest evidence in type 2 inflammation, unifying the heterogeneous pathophysiology of type 2 inflammatory diseases.

IL-4 and IL-13 are key drivers of systemic and local tissue inflammation and mediate different pathophysiologic consequences across type 2 inflammatory diseases (FIGURE 4).1,11,14,21-2


FIGURE 4: IL-4 and IL-13 Are Key Drivers of Systemic and Local Tissue Inflammation.1,11,14,21-28

Identifying Type 2 Inflammation

Recognizing features of type 2 inflammation plays an important role in identification and diagnosis of respiratory diseases such as asthma and CRSwNP, which are predominantly driven by type 2 inflammation.1,29,30

This downloadable checklist can assist clinicians in determining if their patient fits the Global Initiative for Asthma (GINA) criteria for uncontrolled asthma and asthma caused by type 2 inflammation.

Checklist for Severe Uncontrolled Asthma Driven By Type 2 Inflammation

Type 2 inflammation is the most common endotype of inflammation in CRSwNP, driving disease pathology in up to 87% of patients (FIGURE 5).29,30

CRSwNP_Figure 3.png

FIGURE 5: CRS With or Without Nasal Polyps Diagnosis Is Based on Symptoms and Objective Evidence of Disease.31 CRS, chronic rhinosinusitis; EPOS, European Position Paper on Rhinosinusitis; NP, nasal polyps.


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