From the Guidelines
Type 1 and Type 2 inflammation are distinct immune response patterns, with Type 1 targeting intracellular pathogens like viruses and certain bacteria, and Type 2 targeting parasitic infections and involved in allergic reactions, with different cellular mediators and treatments. The key difference between Type 1 and Type 2 inflammation lies in their cellular mediators and purposes, as described in the european position paper on rhinosinusitis and nasal polyps 2020 1.
Key Characteristics of Type 1 and Type 2 Inflammation
- Type 1 inflammation:
- Targets intracellular pathogens such as viruses and certain bacteria
- Involves the activation of Th1 cells, CD8+ T cells, and macrophages
- Produces cytokines like interferon-gamma and TNF-alpha
- Type 2 inflammation:
- Targets parasitic infections, particularly helminths
- Involves Th2 cells, eosinophils, basophils, and mast cells
- Produces cytokines like IL-4, IL-5, and IL-13
Clinical Implications
The distinction between Type 1 and Type 2 inflammation is crucial in clinical practice, as they respond to different treatments, with corticosteroids often being more effective against Type 2 inflammation, and TNF inhibitors being more useful in Type 1 inflammatory conditions, as noted in the study 1.
Treatment Approaches
Understanding the differences between Type 1 and Type 2 inflammation helps guide appropriate therapeutic approaches for inflammatory diseases based on their underlying immunological mechanisms, and the use of biologic agents that target specific aspects of Type 2 inflammation may revolutionize the treatment of chronic rhinosinusitis (CRS) patients with a pure or mixed Type 2 endotype, as discussed in the european position paper on rhinosinusitis and nasal polyps 2020 1.
From the Research
Difference between Type 1 and Type 2 Inflammation
- Type 1 inflammation is characterized by intense phagocytic activity, stimulated by T helper type 1 (Th1) lymphocytes, which secrete interleukin (IL)-2, interferon-gamma, and lymphotoxin-alpha 2.
- Type 2 inflammation is characterized by high antibody titers, stimulated by Th2 cells, which secrete IL-4, IL-5, IL-9, IL-10, and IL-13 2.
- Type 1 immunity is generally protective against most infections, while type 2 responses assist with the resolution of cell-mediated inflammation 2.
- Type 1 cytokines, including IL-2, gamma interferon, IL-12, and tumor necrosis factor beta, favor the development of a strong cellular immune response, whereas type 2 cytokines, including IL-4, IL-5, IL-6, IL-10, and IL-13, favor a strong humoral immune response 3.
- Type 2 immune responses can be either host protective or have pathogenic activity, and are involved in antihelminth immunity, suppression of type 1-driven autoimmune disease, neutralization of toxins, maintenance of metabolic homeostasis, and regulation of wound repair and tissue regeneration pathways 4.
Characteristics of Type 1 and Type 2 Cytokines
- Type 1 cytokines are cross-regulatory, with gamma interferon and IL-12 decreasing the levels of type 2 cytokines, while IL-4 and IL-10 decrease the levels of type 1 cytokines 3.
- Type 2 cytokines induce a complex inflammatory response characterized by eosinophils, mast cells, basophils, type 2 innate lymphoid cells, IL-4-and/or IL-13-conditioned macrophages, and T helper 2 (TH2) cells, which are crucial to the pathogenesis of many allergic and fibrotic disorders 4.
- Eosinophils are involved in combating parasitic, bacterial, viral infections, as well as certain malignancies, and are also implicated in an array of upper and lower respiratory disease states, including asthma, eosinophilic granulomatosis with polyangiitis, and chronic rhinosinusitis with nasal polyposis (CRSwNP) 5.
Therapeutic Strategies for Type 2 Inflammation
- Targeted biologic therapies have revolutionized the treatment of eosinophilic respiratory diseases, including asthma, eosinophilic granulomatosis with polyangiitis, and CRSwNP 5.
- Novel biologics, such as Omalizumab, Mepolizumab, Benralizumab, Reslizumab, Dupilumab, and Tezepelumab, have been developed to target key immunologic pathways affecting type 2 inflammation, including immunoglobulin E (IgE), IL-4, IL-5, IL-13, and upstream alarmins such as thymic stromal lymphopoietin (TSLP) 5.