What is Sensitization?

Previously I explained how asthma is the result of an abnormal immune response. In this post, I aim to delve a little deeper into this subject to show you what researchers have learned (are learning) about the role of the immune system in asthma. I’m going to get a little technical here, but I promise to keep it pithy. I hope to make this complex topic understandable.

In the beginning.

So you were born with asthma genes. Something in your environment activated them, inhaling lots of dust mites daily, perhaps. From now on, when exposed to dust mites, a series of chemical reactions occur inside your body. Worded another way, your asthma genes release proteins that begin a series of biological processes that cause new-onset asthma or, if you already have asthma, trigger asthma symptoms.

The process varies depending on what asthma subgroup you have. For our example here, I’m going to use an allergic asthmatic who is exposed to dust mites.

Ready? Here we go!


This is part of your innate immune system. This is when your immune system recognizes harmless dust mites as harmful. Here is what happens inside your body. Asthmatics and people with allergies too are said to be hypersensitive to allergens. Once this happens, these allergens become antigens.

The difference between allergens, antigens, and pathogens

  • Antigen.  This is any substance your immune system recognizes as harmful. They contain proteins that are recognized as foreign.
  • Pathogens. These are typical antigens. They are proteins that have the potential to be harmful to the human body. They include viruses, bacteria, fungi, and parasites.
  • Allergens. These are atypical antigens. They are proteins that are innocuous (harmless) to the human body.  These include dust mites, pollen, mold spores, cockroach urine, animal dander, certain foods, and non-steroidal anti-inflammatory (NSAID) medicines like Aspirin.
  • T-Lymphocytes (T-Cell). They are white blood cells (leukocytes) that have “antigen-specific receptors” on their surfaces so they can recognize pathogens.1 They are called lymphocytes because they begin developing in bone marrow.2 They hold proteins that are toxic to pathogens, although can also cause inflammation. These proteins are called cytokines and chemokines. T-Cells are made in the bone marrow, although they mature in the thymus, which is what the T stands for (T for Thymus). Once they mature, they circulate the bloodstream looking for pathogens.

There are two types of T-Cells

  1. Killer T-cells. They directly kill pathogens. They are cytotoxic, meaning they kill cells infected with pathogens. I will describe their role in asthma in a future post.
  2. Helper T-Cells. They indirectly kill pathogens. They release proteins that activate other immune cells that can kill. They also activate cells that produce antibodies.1-4

I will define antibodies in a moment.

First, let’s define protein

Proteins. All cells are made of proteins. These include your own cells, and also those in bacteria, viruses, and common allergens, including dust mites, animal dander, cockroach urine, mold spores, and foods. As T-cells scan your body for pathogens, what they are looking for are proteins. They are trained to ignore proteins on your own cells and to only recognize proteins on pathogens. Sometimes, however, they are fooled (perhaps due to asthma genes) into recognizing proteins on allergens as harmful, and these allergens then become antigens (I will explain how this happens in a future post).

Cytokines. They are small proteins. They are the messengers that communicate with cells, telling them to do something. Some are cytotoxic, meaning they damage living cells. Others are chemotaxis, meaning they travel through the blood and recruit white blood cells to the airways (also called positive chemotaxis).4-5

T-helper 1 (Th1) Cells. Their role in (Th2 Dominant Asthma) allergic asthma is not well understood, although it is believed they do play a role in that they “initiate and coordinate cellular immune responses by deploying cytokines such as IL-2 and IFN-g.”6

Interleukin 2 (IL2). It’s made by the IL2 gene and is responsible for the production of T and B Cells.7

Interferon Gamma (IFN-g). It’s made by the IFNg Gene that secretes a cytokine that binds with interferon gamma receptors to increase the immune response to viruses and other microbes. It has been linked to increased incidence of viral and other respiratory infections.8

Dendritic cells. They are antigen-presenting cells in your bloodstream that recognize antigens (in this case dust mites), bind to them, and carry them through your bloodstream to…

T-helper 2 (Th2) cells. They are T-lymphocytes that run the show in asthma. They are the bosses, which is why this response is often called the “Th2 Dominant Inflammatory Response”, or “Th2 Dominant Asthma.” About 50% of asthma cases are said to be Th2 Dominant. When exposed to antigens, they release chemicals into your bloodstream, some of which are…

Interleukin 13 (IL13): It’s a Th2 cytokine that causes airway inflammation, and…9

Interleukin 5 (IL5).  It’s a Th2 cytokine responsible for the growth, activation, and survival of eosinophils. They recruit eosinophils, basophils, and more Th2 cells. These are the recruitments meant to finish off the job of ridding pathogens from your body during the late phase asthma attack that I will cover in an upcoming post.5,10

Interleukin 4 (IL4). It’s a Th2 cytokine made by the IL4 gene and released by T2 cells. They encourage the production of IgE antibodies. They do this by communicating with…5

B-Lymphocytes (B-Cells).  They are also leukocytes. IL4 tells them to release their contents and produce antibodies. In this case, the antibodies created are…6

Dust mite IgE antibodies.  They are specifically trained to recognize dust mite antigen. They roam your bloodstream and can live for many years. Once they appear, you are said to be sensitized to dust mite antigen. A positive allergy test, either via skin prick or blood draw, indicates whether you have these, and an allergy to dust mites. Allergic asthmatics usually have elevated IgE levels.

Conclusion. All of this happens without you even being aware of it, and you feel no symptoms on this day. The response I described here usually occurs in childhood, as you are usually exposed to allergens early in life. Of the other asthma subgroups, some are also initiated in childhood, although most are initiated in adolescence or adulthood.

In either case, by the time all of these events are complete, your body is said to be sensitized to dust mites.

In an upcoming post, I will describe how this sets the stage for asthma attacks. So, stay tuned!

This article represents the opinions, thoughts, and experiences of the author; none of this content has been paid for by any advertiser. The Asthma.net team does not recommend or endorse any products or treatments discussed herein. Learn more about how we maintain editorial integrity here.
View References
  1. Berger, Al, “Th1 and Th2 responses: What are they?” British Medical Journal, August 12, 2000,  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC27457/
  2. . Khan Academy, “Helper T-cells: Immune System Physiology (NCLEX RN),” 2010, Feb. 18, https://www.youtube.com/watch?v=uwMYpTYsNZM, accessed 9/13/17
  3. “T-Cell Modulated Group,” t-cells.org, http://www.tcells.org/beginners/tcells/
  4. Shier, David, Jackie Butler, Ricki Lewis, editors, “Holes Human Anatomy & Physiology,” 7th edition, 1996, page 541, 642
  5.  Deo, et al., “Role played by Th2 type cytokines in IgE mediated allergy and asthma,” lung India, 2010, April-June, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2893428/
  6. Chen, et al., “Stress and Inflammation in Exacerbations of Asthma,” 2007, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2077080/#R24
  7. “IL2 Gene,” Genecards.org, http://www.genecards.org/cgi-bin/carddisp.pl?gene=IL2, accessed 6/27/17
  8. “IFNg Gene,” Genecards.org, http://www.genecards.org/cgi-bin/carddisp.pl?gene=IFNG, accessed 6/27/17
  9.  IL 13.  Perkins, C., “IL-4 induces IL-13 independent allergic airway inflammation,” Journal of Allergy and Clinical Immunology, 2006, August, https://www.ncbi.nlm.nih.gov/pubmed/16890766, accessed 7/7/18
  10. “IL5 Gene (Protein Coding), Genecards, https://www.genecards.org/cgi-bin/carddisp.pl?gene=IL5, accessed 7/7/18