June 22, 2024

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The immunological mechanism of pollen allergy

The immunological mechanism of pollen allergy

The immunological mechanism of pollen allergy. About 40% of people are allergic to pollen and more than 400 million people have symptoms of allergic rhinitis in the world due to hay fever.

Wind plays a key role in pollen sensitization. It makes pollen come into contact with the human upper respiratory tract, eyes and oral mucosa. The moist environment of the mucosa helps release soluble allergens and co-delivers other biologically active compounds combined with the pollen matrix.

Pollen causes allergic rhinoconjunctivitis (“hay fever”), as well as asthma, dermatitis, and food allergies (pollen and food may share allergens).

The immunological mechanism of pollen allergy

The immunological mechanism of pollen allergy

Pollen allergy is mainly a type 1 hypersensitivity reaction. DC cells control the polarization of Naive helper T cells to Th2 and release IL-4, 5, 13 and other Th2 type marker cytokines.

IL-4 plays a key role in the initial stage of sensitization
IL-5 and IL-13 play a key role in the late and effective stages of sensitization. IL-5 is mainly involved in airway eosinophilia and hyperresponsiveness, while IL-13 mainly maintains allergy, recruiting and activating various pathogenic effector cells to the site of allergic inflammation.
Under the action of Th2 cytokines, B cells undergo antibody class switching, produce IgE, bind to the FcεRI on the surface of mast cells and basophils, and then cross-link receptors, causing degranulation and the release of inflammatory factors, triggering allergic symptoms.


The immunological mechanism of pollen allergy (Reference 3)

The pollen of most allergic trees, grasses and weeds (including birch, ryegrass, ragweed, etc.) contains proteolytic enzymes, which can destroy epithelial cells and tight junctions to facilitate the passage of allergens through the epithelial barrier. However, proteolytic enzymes are derived from allergens, or microorganisms carried by allergens, which need further research.

In addition, epithelial cells express TLR4, PARs and other pattern recognition receptors. After binding to allergens, they can release IL-2, 6, 8, TNF-α and other inflammatory factors, as well as alarm elements (IL-25, 33, TLSP) and alarm elements. Induces the expression of OX40L and activates ILC2s to participate in Th2-type cellular immunity.

Pollen characteristics

The common physical and chemical properties of pollen allergens, such as hydrophilicity and post-translational modification, are conducive to bioavailability and uptake by APCs.

Only a few pollen allergens, including Cynd1, Cupal and Amba11, show intrinsic adjuvant activity.

The Cynd1 sugar structure of Bermuda grass pollen can be bound by pattern recognition receptors (C-type lectin receptors).

The cysteine ​​protease activity of the ragweed pollen allergen Amba11 can cause the destruction of airway epithelium and cause Th2 inflammation.

Pollen matrix

Many studies have shown that intact pollen extract has allergenic activity, but if a certain main component is purified, it will no longer have this activity. The possible reason is that the intact extract contains other biologically active ingredients in addition to the pollen itself. Pollen matrix can be divided into two parts, the inherent components of pollen: such as proteins, metabolites, lipids, carbohydrates; foreign components: from air pollutants, virus aerosols and pollen-related microbes.



Allergen-specific immunotherapy

(Allergen‑specific immunotherapy, AIT)

AIT is also called allergy vaccine therapy, using allergenic extracts (such as pollen extract) to make patients tolerate allergens. The mechanism is: regulatory T cells, B cells, and tolerant DC cells induce immune suppression, thereby producing tolerance.

It currently includes subcutaneous injection (SCIT), sublingual oral administration (SLIT) and other preparations.

For how to prepare pollen extract, whether to add adjuvants, and other related adjuvant treatments, please refer to relevant treatment guidelines and commercial products.

For more detailed diagnosis and treatment plans, please refer to: Expert consensus on diagnosis and treatment of allergic diseases in children, etc.