Skip To Main Content

Understanding Type 2 Inflammation

Inflammation does not define you as a person. Have better conversations with your doctor about how to get your disease under control.

TYPE 2 INFLAMMATION - the cause of your condition?

Everyone has a defense mechanism called the type 2 immune response. When your body senses certain types of infections, it sends out specific immune cells - type 2 inflammatory cells - to fight the invaders by creating inflammation.

But for some people, the immune cells go on the attack even when there is no infection, causing damage to the body. This overactive immune response is called type 2 inflammation.

Type 2 inflammation affects one in different ways in different parts of the body, contributing to severe and unpredictable symptoms.

Who experiences type 2 inflammation?

Collage of a woman inhaling on an asthma pump, a woman blowing her nose, and someone scratching their eczema bumps.

Type 2 inflammation is the underlying cause of a number of different diseases. Many of them are called 'atopic,' 'allergic,' or 'eosinophilic'. If you're living with a type 2 inflammatory disease, you're more likely to also have another, driven by the same inflammation.

  • Asthma

  • Skin conditions such as atopic dermatitis (AD)

  • Nasal polyps, or chronic rhinosinusitis with nasal polyposis (CRSwNP)

  • Certain food allergies

Family history and environmental triggers may be the best signs to detect type 2 inflammation, but for some diseases there are also scientific tests.

If you have asthma, ask your doctor about breathing and blood tests to identify the type of inflammation underlying your disease.

Why is it difficult to control?

Environmental triggers can make it worse

The inflammation can damage the body's protected surfaces, such as skin and mucous membranes. Therefore, factors such as allergens, exercise, stress, weather and pollution can lead to type 2 inflammation and cause symptoms to worsen.

 

A long-term problem

Type 2 inflammation is chronic, meaning it is always present in the body, even when symptoms are not felt or seen. Type 2 inflammatory diseases are often first diagnosed in childhood but can develop at any age and can affect people for years or even a lifetime.

 

It can contribute to several diseases

Many people with a type 2 inflammatory disease have additional diseases due to the same underlying inflammation, which can make life even more difficult. Often the more severe disease is diagnosed first.

Several diseases have a connection

Type 2 inflammation affects one in different ways in different parts of the body, contributing to severe and unpredictable symptoms.

It's time to reevaluate your illness and see it from a new perspective. Find out if type 2 inflammation may play a role so you can start asking the right questions.

If you live with AD (a form of eczema), especially moderate to severe forms, you are familiar with the recurring dry, scaly skin and red or dark rashes that cause intense, persistent itching. Many people are diagnosed with this chronic disease as children and experience unpredictable symptoms throughout adulthood.

Because AD affects people so clearly, many people struggle with self-confidence and anxiety. They are often ashamed of their illness and hide their true selves.

Asthma symptoms such as coughing, wheezing and difficulty breathing can limit one's everyday life. Often, asthma attacks are triggered by things in the environment, such as pollen, smoke or even exercise, making it difficult to plan and carry out daily activities.

Have you heard the terms "allergic" or "eosinophilic" to describe your asthma? For people with these types of asthma, type 2 inflammation contributes to the disease.

People with nasal polyps have benign growths in their sinuses. This can lead to a runny nose, difficulty breathing, facial pain and nasal congestion. It can make you feel and look like you are constantly sick.

Many people find that they are losing their sense of smell, which is more than just inconvenient. It can make people miss out on everyday experiences like cooking or eating out and it can make them feel unsafe if they can't detect things like flames or smoke.

Sensitivity to allergens in various foods, such as peanuts, can cause rashes, difficulty breathing, pressure on the chest or throat, and even allergic shock, a life-threatening reaction.

If you have a food allergy, you probably know how difficult it can be to participate in everyday activities, such as eating at a restaurant. This can make the feeling of being "different" even greater.

  1. B. Pulendran, D. Artis, "New paradigms in type 2 immunity," Science, vol. 337, no. 6093, pp. 431-5,  2012.
  2. C.M. Lloyd and R.J. Snelgrove, "Type 2 immunity - Expanding our view," Science Immunology, vol. 3, no. 25, pp. eaat1604, 2018.
  3. T. Zuberbier, S.J. Orlow, A.S. Paller, et al., ”Patient perspectives on the management of atopic dermatitis,” Journal of Allergy and Clinical Immunology, vol.  118, no. 1, pp. 226-232, 2006.
  4. R. Sidbury, W.L. Tom, J.N. Bergman, et al., “Guidelines of care for the management of atopic dermatitis: Section 4. Prevention of disease flares and use of adjunctive therapies and approaches. Journal of the American Academy of Dermatology,” vol. 71, no. 6, pp. 1218-33, 2014.
  5. The Global initiative for Asthma (GINA). GINA PATIENT GUIDE: YOU CAN CONTROL YOUR ASTHMA. 2021. Available at: https://ginasthma.org/wp-content/uploads/2021/05/GINA-Patient-Guide-2021-copy.pdf. Accessed: Oct 2022.
  6. J.I Silverberg, “Comorbidities and the impact of atopic dermatitis,” Annals of Allergy, Asthma & Immunology, vol. 123, no. 2, pp. 144-151, 2019.
  7. D. E. Shaw, A. R. Sousa and S. J. Fowler, “Clinical and inflammatory characteristics of the European U-BIOPRED adult severe asthma cohort,” European Respiratory Journal, vol. 46, no. 5, pp. 1308-1321, 2015.
  8. J.I. Silverberg, J.M. Gelfand, and D.J. Margolis, “Association of atopic dermatitis with allergic, autoimmune, and cardiovascular comorbidities in US adults,” Ann Allergy Asthma Immunol, vol. 121, no. 5, pp. 604-612, 2018.
  9. E. Heffler, F. Blasi and M. Latorre, “The Severe Asthma Network in Italy: Findings and Perspectives.,” Journal of Allergy and Clinical Immunology, vol. 7, no. 5, pp. 1462-1468, 2018.
  10. G. Khan, Vandeplas and Huynh T, “The Global Allergy and Asthma European Network (GALEN rhinosinusitis cohort: a large European cross-sectional study of chronic rhinosinusitis patients with and without nasal polyps,” Rhinology, vol. 57, no. 1, pp. 32-42, 2019.
  11. J.C. Staniorski, C.P.E. Price, and A.R. Weibman, “Asthma onset pattern and patient outcomes in a chronic rhinosinusitis population,” Int Forum Allergy Rhinol, vol. 8, no. 4, pp. 495-503, 2018.
  12. C. Philpott, S. Erskine and C. Hopkins, “Prevalence of asthma, aspirin sensitivity and allergy in chronic rhinosinusitis: data from the UK National Chronic Rhinosinusitis Epidemiology Study,” Respiratory Research, vol. 19, p. 129, 2018.
  13. D. Bonamonte, A. Filon,i M. Vestita, “The Role of the Environmental Risk Factors in the Pathogenesis and Clinical Outcome of Atopic Dermatitis”, Biomed Res Int, vol. 2019, art. 2450605, 2019.
  14. W. Cookson, “The alliance of genes and environment in asthma and allergy”, Nature, vol. 25, no. 402(6760 Suppl), pp. B5-11, 1999.
  15. J.N. Liu, et al, “The prevalence of serum specific IgE to superantigens in asthma and allergic rhinitis patients,” Allergy, Asthma & Immunology Research, vol. 6, no.3, pp. 263-266, 2014.
  16. R.P. Schleimer and S. Berdnikovs, “Etiology of epithelial barrier dysfunction in patients with type 2 inflammatory diseases,” Journal of Allergy and Clinical Immunology, vol. 139, no. 6:1752-1761, 2017.
  17. J. Arndt, N. Smith and F. Tausk, “Stress and atopic dermatitis”, Curr Allergy Asthma Rep, vol. 8, no. 4, pp. 312-7, 2008.
  18. M. Tsuge, M. Ikeda, N. Matsumoto, et al. “Current Insights into Atopic March”, Children (Basel), vol. 19; no. 8(11), pp. 1067, 2021.
  19. L.F. Eichenfield, et al., "Guidelines of care for the management of atopic dermatitis: section 1. Diagnosis and assessment of atopic dermatitis," Journal of the American Academy of Dermatology, vol. 70, no. 2, pp. 338-351, 2014.
  20. N. Maison, et al, "T2-high asthma phenotypes across lifespan,” European Respiratory Journal, vol. 60, no. 3, pp. 2102288, 2022.
  21. European Forum for Research and Education in Allergy and Airway Diseases. 2022. https://www.euforea.eu/crswnp. Accessed Oct 2022.
  22. S. Nordin, H. Blomqvist, P. Olsson, et al., “Effects of smell loss on daily life and adopted coping strategies in patients with nasal polyposis with asthma.” Acta oto-laryngologica, vol. 131, no. 8, pp. 826-32, 2011.
  23. N. Saydy, P. Moubayed and M. Desrosiers, "Patient perspectives on endoscopic sinus surgery for chronic rhinosinusitis,” Journal of Otolaryngololy Head Neck Surgery, vol. 50, no. 34, 2021.
  24. C. Prussin, J. Lee J, B. Foster, “Eosinophilic gastrointestinal disease and peanut allergy are alternatively associated with IL-5+ and IL-5− TH2 responses,” Journal of allergy and clinical immunology, vol. 124, no. 6, pp. 1326-32, 2009.