Cat and pollen allergies and asthma: atopy through the lens of genetics

A woman with a mug sitting by a window next to a white cat, looking at blooming spring trees — main cover image for the article on atopy genetics.

The predisposition to allergic rhinitis, reactions to animals, and asthma is described by the common term “atopy,” yet different biological mechanisms lie behind this label. What these conditions share is a type 2 response — the coordinated action of a group of immune signaling molecules that leads to the production of IgE antibodies and inflammation of the mucous membranes. The genetic architecture, however, is not uniform: individual variants shift susceptibility to different links in this response, while the environment and the form of the disease determine how it actually manifests. Genetics makes it possible to break the shared pattern down into distinct biological components.

Why Cat, Pollen, and Asthma Allergies Can Occur Together in One Person

Allergic rhinitis, reactions to animals, and asthma can occur in one person because of a predisposition to allergic sensitization — a state in which the immune system produces specific IgE antibodies against substances that do not normally trigger an immune response.

This mechanism distinguishes allergy from intolerance, and you can read more about it in the article Food Allergy and Intolerance: How to Tell Them Apart and What to Do.

In some people, manifestations of atopy appear sequentially, starting with the skin: atopic dermatitis in early childhood, then allergic rhinitis, and later asthma. This sequence is described by the term “the atopic march.” Genetic research data show that shared risk loci (genome regions associated with a trait) reflect the contribution of hereditary factors to the sequential development of allergic conditions, while loci unique to individual diseases explain the tissue-specific nature of their manifestations (Lawson et al., J. Allergy Clin. Immunol., 2025).

This sequence is not obligatory and can vary: manifestations may appear in a different order, be limited to a single organ, or not develop at all. At the same time, asthma is not a form of allergy: it is heterogeneous in age of onset, the nature of airway inflammation, and response to treatment, and allergic sensitization accompanies only some of its forms (Porsbjerg et al., Lancet, 2023).

Close-up of microscopic allergen particles and pollen floating in sunlight near a window frame.

What Happens in the Airways When the Body Reacts to an Allergen

The reaction to an allergen begins at the epithelium — the layer of cells lining the airways. Epithelial cells recognize allergen components through innate immunity receptors. For instance, the mite allergen Der p2 activates the TLR-4 receptor, which responds to structures characteristic of microorganisms, while serine proteases from pollen and mites act through the PAR-2 receptor, which is sensitive to protein cleavage (Gauvreau et al., Allergy, 2023).

Once activated, epithelial cells release alarmins — signaling molecules that include thymic stromal lymphopoietin (TSLP) and interleukin-33. Alarmins trigger the type 2 response and cause various effector cells to produce the cytokines IL-4 and IL-13 (Gauvreau et al., Allergy, 2023).

Interleukins IL-4 and IL-13 transmit the signal into the cell via the JAK-STAT pathway — a cascade of proteins that carries the signal from a receptor on the cell surface to its nucleus and changes gene activity. The strength and nature of this signal depend on other intracellular programs operating in the cell at the same time (Shankar et al., J. Allergy Clin. Immunol., 2022). The result of this stage is the switching of B lymphocytes to IgE production, eosinophilic inflammation, and increased mucus production in the airways (Gauvreau et al., Allergy, 2023). IgE then binds to high-affinity receptors on mast cells, and repeated contact with the allergen triggers the release of mediators that cause nasal congestion, sneezing, coughing, and bronchospasm.

What Genetic Mechanisms Shape Susceptibility to Different Atopic Manifestations

Genome-wide association studies (GWAS) have identified 212 risk loci for allergic sensitization. Most of them (136 loci) are associated simultaneously with atopic dermatitis, asthma, food allergy, and allergic rhinitis. In other words, these conditions do share a common genetic basis. The identified variants are located mostly in non-coding regions, so they most likely affect gene activity regulation rather than altering protein structure (Lawson et al., J. Allergy Clin. Immunol., 2025). Because the trait is quantitative and depends on many variants with small effects, their combined contribution is summarized by a polygenic risk score (PRS), which, when used in genetic research, shows a person's position relative to a reference population.

The genes located within the risk loci operate at different stages of the response described above. The gene TSLP (thymic stromal lymphopoietin) encodes an alarmin that initiates the response at the epithelial level. The gene IL13 (interleukin 13) encodes one of the key type 2 cytokines, while the gene IL4R (interleukin 4 receptor) encodes the receptor subunit through which the IL-4 and IL-13 signal enters the cell. The gene FCER1A (Fc epsilon receptor Ia) encodes the alpha chain of the high-affinity IgE receptor, meaning it operates at the effector stage.

Some of the genetic factors behind asthma lie outside the response described above. The 17q21 locus, which contains the gene GSDMB (gasdermin B), is among the strongest signals linked to childhood-onset asthma and has been confirmed across many independent samples (Jakwerth et al., Am. J. Respir. Crit. Care Med., 2024). The effect of this locus is linked to increased vulnerability of the airway mucosa to respiratory viruses and a weakened interferon antiviral response. This mechanism operates outside allergic sensitization, meaning asthma has its own hereditary risk factors that are unrelated to allergic predisposition.

A toddler playing with a toy train on the floor by a large window next to a gray cat in a bright room.

How the Environment Affects the Expression of Atopic Predisposition

Carrying variants associated with an increased likelihood of atopy does not mean the condition will develop: this depends on the conditions in which a person grows up and lives. Asthma forms under the influence of numerous genetic and environmental factors and their interaction throughout life, rather than at a single moment (Koppelman et al., Lancet Respir. Med., 2025).

One explanation for why such conditions have become more common links the rising prevalence of allergic conditions to damage to the epithelial barrier caused by substances that have increased alongside industrialization and urbanization (Akdis, Nat. Rev. Immunol., 2021).

For carriers of 17q21 variants associated with an increased risk of asthma, respiratory viral infections experienced in the first years of life matter: it is precisely at this link that the increased mucosal vulnerability manifests (Jakwerth et al., Am. J. Respir. Crit. Care Med., 2024). Smoking, polluted air in large cities, harmful working conditions, and excess weight are also among the factors that influence the likelihood of developing asthma (Koppelman et al., Lancet Respir. Med., 2025).

What Genetic Factors of Allergic Predisposition Can Be Seen in the Report

The results of genetic testing describe a stable hereditary component of predisposition — variants linked to the workings of type 2 response signaling links and IgE regulation. Laboratory tests, in turn, answer a different question. Specific IgE and skin tests show exactly which allergens allergic sensitization has formed against at the time of testing. Genetic data does not replace this information: it describes predisposition, while examinations help explain the current state.

Genetic factors linked to allergic predisposition can be analyzed with Apixmed Prism DNA tests: the relevant indicators are included in the report together with other areas exploring the body's reactions to external factors.

For more on the analysis of such predispositions and risks, see the article “Allergies, Intolerances, and DNA: What a Genetic Test Reveals About Your Body's Reactions” (No. 57).

How to Understand the Combination of Allergic Manifestations

A shared origin of predisposition is not grounds for considering the described allergic conditions to be a single disease: each has its own course, specific triggers, and a corresponding management approach. At the same time, this shared predisposition explains why these conditions can occur together.

This applies most of all to asthma. The disease requires separate assessment even when allergy is confirmed: the form, age of manifestation, and nature of inflammation determine treatment, while allergic sensitization is only one of the possible mechanisms behind the disease's development.

The genetic result describes the hereditary component of predisposition. Manifestations change with the season, age, and living conditions, while the genetic component remains constant. The percentile reflects how much your genetic predisposition differs from that of most people, not the probability that you will develop a specific condition. Decisions about testing and treatment are made based on symptoms and examination results, which are evaluated by an allergist or pulmonologist.

To complement your test results with hereditary context, explore Apixmed Prism tests,

The results of a genetic test are not a diagnosis and do not replace a doctor's consultation. The Apixmed Prism report provides genetic context that complements examination results and helps you make decisions together with your doctor.

Sources

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