Guide · 7 min
Why Your Immune System Overreacts — And How It Can Learn to Stop
The surprisingly retrainable biology behind hayfever
In short
Th2 immune dominance in allergic rhinitis is driven by a coordinated cascade initiated at epithelial barrier disruption, where allergen proteases, lipids, and extracellular vesicles activate innate immune signals that bias dendritic cells toward Th2-polarizing antigen presentation. This triggers…
Your immune system isn't broken — it's just miscalibrated
If you've ever wondered why your body treats a drifting grass pollen grain as if it were a dangerous pathogen, you're asking exactly the right question. Hayfever isn't a weakness or an overreaction in any moral sense. It's the result of a series of remarkably precise biological decisions — made largely before you were old enough to sneeze — that set your immune system onto a particular path. Understanding that path is the first step toward getting ahead of it.
This is the story of how Th2 immune dominance takes hold, why your mast cells become hair-trigger sensitive, what your IgE levels actually mean, and — perhaps most encouragingly — why the immune system that learned to overreact can, in the right circumstances, be taught to stand down.
The science: how an immune system tips Th2
The early-life window that shapes everything
Your immune system faces a fundamental choice when it first encounters an allergen: mount a defensive response, or learn to tolerate it. The direction it chooses — and this is the critical part — is largely determined very early in life.
Peter Holt's landmark 1997 developmental research established that allergen-specific immune memory is laid down during a narrow window around first exposure, and that this early Th2-skewed sensitisation can confer lifelong immune polarisation (Holt, 1997). This isn't destiny written in stone, but it does mean the immune architecture you carry into adulthood has deep roots.
The cytokine cast: IL-4, IL-5, IL-13, and the signalling cascade
Once sensitisation occurs, allergic rhinitis is driven by a specific ensemble of signalling molecules — cytokines — that orchestrate inflammation with considerable precision. The primary players are IL-4, IL-5, and IL-13 (Ngoc et al., 2005; Broide, 2010; Pawankar et al., 2011).
- IL-4 drives IgE class-switching in B cells and upregulates adhesion molecules that help eosinophils migrate into nasal tissue
- IL-5 sustains the survival and recruitment of eosinophils — the white blood cells responsible for much of the tissue inflammation
- IL-13 activates STAT6 signalling, triggering goblet cell hyperplasia and the mucus overproduction that gives rise to rhinorrhoea and congestion
But these cytokines don't arrive from nowhere. Upstream of them sits a set of epithelial 'alarm signals' — TSLP, IL-33, and IL-25 — released when the nasal barrier is damaged or irritated by allergen exposure. These alarmins condition dendritic cells and activate innate lymphoid cells (ILC2s), which then push the adaptive immune system firmly into Th2 mode (Albloushi & Al-Ahmad, 2023). Think of the alarmins as the starting gun and the Th2 cytokines as the race itself.
Why isn't there a counter-force?
A healthy immune system maintains balance through competing signals. Th1 responses (driven by IFN-γ and IL-12) and regulatory T cells normally provide a brake on Th2 activity. In allergic rhinitis, this dual counter-regulation fails. The Th2-produced cytokine IL-10 suppresses IFN-γ, removing the principal Th1 brake on IgE production. Simultaneously, regulatory T cells (Tregs) are reduced or dysfunctional in people with allergic rhinitis compared to healthy controls (Nouri-Aria & Durham, 2008).
Venarske and deShazo (2003) noted that this is not simply a Th1 deficiency — it is a compound failure of both Th1 and T-regulatory mechanisms operating together. Reduced microbial stimulation in early life, as the hygiene hypothesis suggests, impairs both arms of this counter-regulation, creating an environment where Th2 responses meet little resistance.
The mast cell: your body's hair-trigger alarm
At the sharp end of allergic symptoms sits the mast cell — a tissue-resident immune cell that, once sensitised, can release a torrent of inflammatory mediators within minutes of allergen encounter.
The mechanism is elegant in its precision and frustrating in its consequences. Allergen-specific IgE, produced through Th2-driven signalling, binds to high-affinity FcεRI receptors on mast cell surfaces. The cell is now 'armed'. When the same allergen appears again and crosslinks these IgE-FcεRI complexes, a Lyn/Syk kinase signalling cascade fires, driving rapid degranulation of preformed mediators — histamine, tryptase — and de novo synthesis of leukotrienes and prostaglandins. The familiar symptoms of sneezing, itching, and nasal congestion follow within minutes (Vitte et al., 2022; Gilfillan et al., 2009).
What makes mast cells hypersensitive in atopic individuals is a combination of factors. FcεRI receptor density is 2- to 100-fold higher in people with atopy, meaning far more IgE can be loaded onto each cell's surface. Priming cytokines — IL-33, IL-4, and stem cell factor (SCF) — further lower the activation threshold without directly triggering degranulation, so the cell responds to allergen doses that would be harmless in a non-sensitised person. Repeated seasonal exposure maintains this state through a self-reinforcing loop: more allergen drives more IgE, which arms more mast cells, which produce more inflammatory cytokines, which lower activation thresholds further (Ando & Kitaura, 2021).
There is also an IgE-independent pathway worth noting. The receptor MRGPRX2 responds to neuropeptides such as substance P, contributing to what are sometimes called pseudo-allergic or neurogenic responses — a finding that helps explain why stress, exercise, and cold air can trigger mast cell reactions even in the absence of allergen (Ebo et al., 2022).
What your IgE levels actually mean
You may have had an IgE blood test and wondered what the numbers signify for how you'll feel on a high-pollen day. The science here offers a nuanced answer.
Allergen-specific IgE (sIgE) does show a meaningful dose-dependent relationship with symptom severity — particularly for grass pollen and house dust mite sensitisation. Corsico et al. (2017) found significant differences in sIgE levels across ARIA (Allergic Rhinitis and its Impact on Asthma) severity grades, with higher sIgE correlating with more severe and persistent symptoms.
However, total IgE — the kind most commonly measured in routine blood panels — shows weak or no correlation with symptom severity. This makes biological sense: total IgE captures all IgE regardless of what it binds to, while it's the specific IgE molecules targeting your personal sensitising allergens that actually arm the mast cells responsible for your symptoms. One important caveat: Nickeisen et al. (1986) found that even sIgE levels don't perfectly predict symptom severity in all patients, a reminder that your subjective experience is shaped by allergen exposure levels, polysensitisation, and individual mast cell reactivity, not IgE titre alone.
What this means for you
If you've been living with hayfever, several things follow from this biology.
First, your symptoms on any given day reflect not just today's pollen count but the accumulated state of your immune system — the density of armed mast cells in your nasal mucosa, the current Th2/Treg balance, and the load of allergen-specific IgE bound to those cells. This is why you can feel fine for the first week of the grass season and then suddenly be floored by the same pollen levels a fortnight later: your mast cells have had time to reprime.
Second, the alarmins TSLP and IL-33 are released whenever the nasal epithelial barrier is disrupted — which means anything that irritates your nose (cold, dry air, air pollution, cigarette smoke) can amplify your allergic response to pollen even when pollen levels are moderate. Your barrier integrity matters.
Third, and most importantly: the biology described here is not fixed. The same mechanisms that drive Th2 dominance — Treg suppression, IgE production, mast cell priming — are, in principle, reversible.
Can the immune system be retrained? The case for tolerance
This is where the science becomes genuinely encouraging.
Some people do outgrow allergies naturally. The mechanism mirrors what allergen immunotherapy achieves deliberately: sustained allergen exposure under the right immunological conditions promotes expansion of allergen-specific regulatory T cells, which suppress Th2 cytokine production via IL-10 and TGF-β, while shifting B-cell isotype switching away from IgE toward non-inflammatory IgG4 blocking antibodies. The result is a progressive raising of the mast cell activation threshold (Akdiş, 2009; Çelebi Sözener et al., 2020).
Allergen-specific immunotherapy (AIT) — delivered as subcutaneous injections or sublingual drops/tablets — is the only currently licensed treatment that exploits this mechanism deliberately, and the evidence base is strong. Multiple RCTs and meta-analyses demonstrate 40–60% symptom reduction, with effects that persist for years after treatment cessation — a disease-modifying result that antihistamines and nasal steroids simply cannot match (Schmidt-Weber & Blaser, 2005; Satitsuksanoa et al., 2022).
The mechanism involves induction of Foxp3+ Tregs and IL-10-producing Tr1 cells that suppress dendritic cell costimulation, dampen Th2 cytokine secretion, and shift the immunological balance toward tolerance. Restoration of Treg function through AIT correlates directly with symptom improvement across multiple studies (Nouri-Aria & Durham, 2008; Luo, 2012).
The evidence landscape: what we know and what we don't
It's worth being honest about the limits of this science.
The core mechanisms — IgE, FcεRI signalling, Th2 cytokines, Treg suppression — are well-established and supported by converging evidence across cell biology, human studies, and clinical trials. Confidence in these findings is high.
Where the picture becomes hazier:
- Epigenetics and transcription factors. The precise roles of GATA-3, STAT6, and epigenetic regulation in locking in Th2 commitment are not fully characterised, particularly with respect to newer pathogenic Th2A cell subsets.
- ILC2 biology. Innate lymphoid cell type 2 contributions are an active research frontier; how they interact with classic adaptive Th2 responses under real-world exposure conditions remains incompletely characterised.
- sIgE thresholds. We don't yet have well-validated sIgE cut-offs that reliably predict symptom severity at the individual level across diverse populations and allergen types.
- Natural tolerance resolution. Precise outgrowth rates for aeroallergens like pollen are poorly quantified in prospective studies, making it difficult to counsel individuals on whether their hayfever is likely to resolve with age.
- Novel immunotherapies. Treg-based cell therapies and so-called 'inverse vaccines' show mechanistic promise but currently lack peer-reviewed clinical trial data in allergic rhinitis specifically.
What Haelo recommends
Grounded in this evidence, here's how to translate the biology into meaningful action:
1. Understand your sensitisation profile, not just your total IgE. If you've only ever had total IgE measured, ask your GP or allergist about allergen-specific IgE testing or a skin-prick panel. Knowing which allergens you're actually sensitised to — and at what titre — gives you far more useful information for planning your season.
2. Protect your nasal barrier proactively. Because TSLP and IL-33 release begins when the epithelial barrier is disrupted, using a nasal saline rinse or barrier spray during peak season can reduce alarmin signalling before it starts — keeping the mast cell 'starting gun' from firing as readily.
3. Start antihistamines before symptoms peak, not after. Knowing that mast cells build up allergen-specific IgE loading over the early season, pre-treating with a non-sedating antihistamine in the days before your personal pollen threshold typically tips is more effective than waiting for the cascade to begin.
4. If your symptoms are moderate to severe, ask about AIT. If you find yourself relying on multiple medications for several months a year, allergen immunotherapy is the only intervention with evidence for disease modification. It requires commitment (typically 3 years), but the evidence for lasting reduction in both symptoms and medication use is robust. This is a conversation worth having with a specialist.
5. Track your symptoms longitudinally. Because the Th2/Treg balance and mast cell priming state change across a season and across years, logging your symptoms alongside pollen data helps you — and Haelo — identify patterns that one-off assessments miss. The immune system is dynamic; your intelligence about it should be too.
The science of allergic immunity is advancing rapidly, and Haelo's evidence base is continuously updated as new research emerges. The findings described here represent the current state of moderate-to-strong consensus, with uncertainty honestly noted where it exists.
The evidence
What the research actually says
Each answer below is drawn from a graded research review. Confidence reflects the strength of the underlying evidence, not how confident we feel about it.
What drives Th2 immune dominance?
Th2 immune dominance in allergic rhinitis is driven by a coordinated cascade initiated at epithelial barrier disruption, where allergen proteases, lipids, and extracellular vesicles activate innate immune signals that bias dendritic cells toward Th2-polarizing antigen presentation. This triggers naive CD4+ T cell differentiation via IL-4/STAT6/GATA-3 signaling, establishing Th2 lineage commitment and sustained production of IL-4, IL-5, and IL-13, which collectively orchestrate IgE class switching, eosinophil recruitment, and mucus hypersecretion. Reciprocal suppression of Th1 responses through IL-10 and IL-6-mediated IFN-γ inhibition self-reinforces and stabilizes the Th2-dominant state.
How it works
IL-4 activates STAT6, which upregulates the master transcription factor GATA-3, locking CD4+ T cells into Th2 lineage commitment and driving autocrine amplification of the Th2 cytokine program; simultaneously, allergen-derived proteases disrupt epithelial tight junctions and activate protease-activated receptor-2, generating oxidative stress signals and innate alarmins that prime the upstream dendritic cell environment toward Th2 polarization before adaptive responses are engaged.
Confidence: high
Why do mast cells become hypersensitive?
Mast cell hypersensitivity develops primarily through IgE-dependent upregulation of the high-affinity receptor FcεRI, where increasing IgE levels drive 2-5 fold increases in surface FcεRI expression, lowering the allergen threshold for degranulation by approximately 10-fold and amplifying mediator release (e.g., 73% more histamine, 156% more LTC4). Sensitization occurs when allergen crosslinks IgE-FcεRI complexes, triggering rapid release of preformed mediators (histamine, tryptase, TNF-α) and de novo synthesis of lipid mediators and cytokines (IL-4, IL-13, PGD2). Additional amplification arises from non-IgE pathways including innate receptor signaling (TLRs, ST2/IL-33), galectin-3 crosslinking, and neuropeptides such as substance P, collectively sustaining feedforward hypersensitivity loops.
How it works
Upon allergen re-exposure, crosslinking of IgE-occupied FcεRI receptors triggers ITAM-mediated phosphorylation cascades (amplified ~100-fold by the FcεRIβ subunit), rapidly activating downstream signaling (Lyn, Syk, PLCγ) that drives degranulation and cytokine synthesis; the resulting IL-4/IL-13 promote further local IgE production and Th2 skewing, while TNF-α matures dendritic cells, creating a self-reinforcing sensitization cycle.
Confidence: moderate
How do IgE levels correlate with symptoms?
Allergen-specific IgE (sIgE) demonstrates a meaningful but imperfect correlation with allergic rhinitis symptom severity, with high sIgE levels (>50 kU/L) associated with approximately 2-fold greater symptom burden in untreated patients. In contrast, total serum IgE shows inconsistent and generally unreliable correlation with symptom severity across multiple studies spanning nearly four decades, from Nickeisen et al. (1986) to recent 2024-2025 investigations. The relationship is further complicated by patient age, sensitization pattern, allergen exposure, and disease phenotype (seasonal vs. perennial).
How it works
Allergen-specific IgE sensitizes mast cells and basophils via high-affinity FcεRI receptors; upon allergen re-exposure, crosslinking of bound sIgE triggers degranulation and release of histamine, leukotrienes, and cytokines, directly driving nasal symptoms — explaining why sIgE quantity is more mechanistically linked to symptom intensity than polyclonal total IgE. Total IgE reflects broader atopic burden and non-specific sensitization, diluting its predictive signal for any single allergen-driven symptom response.
Confidence: moderate
Which cytokines drive allergic rhinitis symptoms?
Strong and consistent evidence from multiple mechanistic reviews and clinical studies identifies IL-4, IL-5, IL-13, IL-33, and TSLP as the primary cytokines driving allergic rhinitis symptoms, operating through a Th2-skewed inflammatory cascade. IL-4 and IL-13 promote IgE production and mucus hypersecretion, IL-5 drives eosinophil recruitment and tissue damage, while epithelial alarmins IL-33 and TSLP amplify the response via dendritic cell conditioning and ILC2 activation. Additional mediators including TNF-α, GM-CSF, and TGF-β contribute to disease severity, with quantitative data showing serum IL-4 levels 2.1–2.8 times higher in AR patients versus controls.
How it works
Allergen exposure cross-links IgE on sensitized mast cells, triggering immediate histamine/leukotriene release and subsequent Th2 cytokine secretion (IL-4, IL-5, IL-13) that sustains late-phase eosinophilic inflammation and goblet cell hyperplasia; concurrently, epithelial barrier damage releases alarmins (IL-33, TSLP) that condition dendritic cells for Th2 priming and activate ILC2s, creating a self-amplifying inflammatory loop responsible for nasal congestion, rhinorrhea, and sneezing.
Confidence: high
Why do some people outgrow allergies?
Some individuals naturally outgrow allergies through the development of allergen-specific immune tolerance, driven primarily by regulatory T cells (Tregs/Tr1 cells) and regulatory B cells (Br1 cells) that actively suppress pathological Th2 responses. The shift toward tolerance is characterized by increased IL-10 production, IgG4 class switching, and the generation of allergen-specific memory B cells — mechanisms documented both in spontaneous tolerance and therapeutically-induced tolerance via immunotherapy. Evidence from cow's milk allergy specifically shows that children who naturally outgrow the allergy exhibit increased frequencies of circulating allergen-specific B cells, paralleling changes seen with oral immunotherapy.
How it works
IL-10-secreting Tr1 regulatory T cells suppress allergic responses by inhibiting CD28/ICOS-dependent T cell costimulation, downregulating MHC class II on antigen-presenting cells, and driving B cells toward IgG4 production rather than IgE; IgG4 acts as a non-inflammatory 'blocking' antibody that competes with IgE at mast cell and basophil receptors, thereby preventing degranulation and allergic symptoms. Regulatory B cells further reinforce this tolerogenic state through antigen-specific suppression.
Confidence: moderate
Can immune tolerance be retrained?
Yes, immune tolerance can be retrained through allergen-specific immunotherapy (AIT), which is currently the only treatment modality demonstrated to alter the natural course of allergic diseases including allergic rhinitis. Multiple high-quality RCTs and systematic reviews confirm that ≥3 years of AIT (subcutaneous or sublingual) produces durable, disease-modifying tolerance that can persist for years after treatment cessation, with symptom-medication score improvements of approximately 50-70% versus placebo. Shorter courses (e.g., 2 years) yield only transient benefits, underscoring the importance of treatment duration for sustained immunological reprogramming.
How it works
AIT retrains immune tolerance through three converging mechanisms: induction and expansion of allergen-specific regulatory T cells (Tregs, both FOXP3+CD4+CD25+ and IL-10/TGF-β-producing Tr1 cells) that suppress Th2-driven allergic inflammation; a class-switch from pathogenic IgE to blocking IgG4 antibodies (up to 100-fold increase) that competitively inhibit allergen-IgE binding on mast cells and basophils; and progressive desensitization of mast cells and basophils, reducing histamine release and downstream effector responses.
Confidence: high
What regulates mast cell activation thresholds?
Mast cell activation thresholds are regulated by a dynamic balance between activating and inhibitory signaling networks converging on FcεRI. Inhibitory receptors (FcγRIIB, SHIP1) raise thresholds by dampening PI3K/Akt and Ca²⁺ signaling, while co-stimulatory inputs from cytokines (IL-33, SCF, IL-4), GPCRs, and TLR ligands lower thresholds by priming FcεRI expression and downstream Syk/LAT/PLCγ signaling. IgE sensitization levels further modulate thresholds by increasing FcεRI surface density, reducing the antigen concentration required to trigger degranulation by up to 100-fold.
How it works
FcεRI crosslinking initiates Syk-dependent phosphorylation of LAT, activating PLCγ to generate IP₃ and DAG, which mobilize intracellular Ca²⁺ and activate PKC/MAPK cascades required for degranulation; this threshold is raised by SHIP1-mediated PIP₃ hydrolysis downstream of inhibitory FcγRIIB co-ligation, and lowered by PI3K amplification via co-stimulatory receptors and cytokine-induced upregulation of proximal signaling components.
Confidence: high
Do regulatory T cells reduce allergic symptoms?
Regulatory T cells (Tregs) play a significant role in suppressing allergic rhinitis symptoms, with multiple studies demonstrating that AR patients exhibit reduced circulating Treg numbers and impaired Treg function compared to healthy controls. Allergen-specific IL-10-secreting Tr1 cells are notably decreased in persistent AR, and allergen immunotherapy (SIT) works in part by enhancing Treg immunosuppressive activity and increasing circulating Treg populations. The Th17/Treg imbalance is now recognized as a key pathogenic axis in AR, with restoration of this balance representing a therapeutic target.
How it works
Tregs suppress Th2-driven allergic inflammation primarily through secretion of IL-10, TGF-β, and IL-35, which inhibit IgE production, mast cell and eosinophil activation, and effector T/B cell proliferation while promoting immunoglobulin class switching toward IgG4/IgA. Additional suppression occurs via cell-contact-dependent mechanisms including CTLA-4 and CD39/CD73 signaling, and follicular Tregs (Tfr) limit IgE production by inhibiting Tfh-B cell interactions.
Confidence: moderate
Where the evidence runs out
The precise role of innate lymphoid cells type 2 (ILC2s) as upstream amplifiers of Th2 polarization independent of T cell receptor signaling is not well-characterized in the reviewed literature, representing a significant mechanistic gap. Additionally, quantitative clinical data on cytokine thresholds, epigenetic mechanisms of GATA-3 stabilization, and the relative contributions of different environmental cofactors (microbiome, vitamin D, lipid adjuvants) to Th2 dominance in vivo remain insufficiently defined. Most quantitative threshold data (FcεRI density changes, mediator release amplification) derive from in vitro cell lines (e.g., LAD2) and rodent knockout models, with limited human in vivo validation of these thresholds in atopic tissues. Long-term cytokine dynamics governing chronic hypersensitivity maintenance, as well as the relative contributions of IgE-independent innate pathways in clinical allergic rhinitis specifically, remain incompletely characterized. Most studies are limited by modest sample sizes, cross-sectional designs, and heterogeneous severity classification systems (ARIA, VAS, Danyoung), making direct comparisons difficult. The relative contribution of local nasal IgE versus serum IgE to symptom severity remains insufficiently characterized, and large-scale prospective studies controlling for allergen exposure levels and polysensitization are lacking. Most evidence derives from observational cytokine profiling studies and mechanistic reviews rather than large interventional RCTs, leaving longitudinal threshold data for IL-33 and TSLP, head-to-head comparisons across AR severity subgroups, and direct therapeutic targeting (e.g., anti-IL-5, anti-IL-33) in pure AR populations insufficiently characterized. The relative contributions of individual cytokines versus their network interactions, and how these profiles differ between seasonal and perennial AR, require further systematic investigation. The available evidence largely derives from immunotherapy studies and mechanistic reviews, with limited longitudinal data on spontaneous, untreated allergy resolution — including prevalence rates, age-related immune maturation factors, allergen-specific timelines, and whether epitope spreading plays a distinct role in natural versus therapy-induced tolerance acquisition. Long-term relapse rates beyond 5 years remain incompletely characterized, with some cohorts reporting ~20-30% recurrence, and the precise thresholds of Treg induction or IgG4 levels required for durable tolerance lack validated clinical biomarkers. Mechanistic data on mast cell desensitization in humans rely largely on indirect measures, and epitope-specific T-cell therapies remain insufficiently tested outside grass pollen models. Most quantitative threshold data derive from in vitro BMMC or RBL-2H3 models, leaving in vivo human-specific threshold values and the relative contribution of each regulatory axis in intact tissue microenvironments poorly characterized. Additionally, the interplay between lipid raft dynamics, TRP channel activity, and cytoskeletal remodeling in setting physiological degranulation thresholds lacks systematic in vivo validation. Most human studies are small, cross-sectional, and observational, limiting causal inference; large randomized trials directly quantifying symptom reduction via Treg biomarkers are lacking. Long-term persistence of Treg functional changes following allergen immunotherapy remains poorly characterized, and discrepancies in Treg suppressive function between allergic rhinitis and allergic asthma subjects suggest disease-context-specific variability that is not yet fully understood.
References
- 1.Holt P. · 1997 · Development of sensitization versus tolerance to inhalant allergens during early life
- 2.Ngoc LP, Gold DR, Tzianabos AO et al. · 2005 · Cytokines, allergy, and asthma
- 3.Venarske D, deShazo R. · 2003 · Molecular mechanisms of allergic disease
- 4.Broide D. · 2010 · Allergic rhinitis: Pathophysiology
- 5.Pawankar R, Mori S, Ozu C et al. · 2011 · Overview on the pathomechanisms of allergic rhinitis
- 6.Albloushi S, Al-Ahmad M. · 2023 · Exploring the latest understanding on the role of immune mediators, genetic and environmental factors in pathogenesis of allergic rhinitis: a systematic review
- 7.Vitte J, Vibhushan S, Bratti M et al. · 2022 · Allergy, Anaphylaxis, and Nonallergic Hypersensitivity: IgE, Mast Cells, and Beyond
- 8.Gilfillan AM, Peavy RD, Metcalfe DD. · 2009 · Amplification mechanisms for the enhancement of antigen-mediated mast cell activation
- 9.Ando T, Kitaura J. · 2021 · Tuning IgE: IgE-Associating Molecules and Their Effects on IgE-Dependent Mast Cell Reactions
- 10.Ebo DG, Beyens M, Heremans K et al. · 2022 · Recent Knowledge and Insights on the Mechanisms of Immediate Hypersensitivity and Anaphylaxis: IgE/FcεRI- and Non-IgE/FcεRI-Dependent
- 11.Corsico AG, De Amici M, Ronzoni V et al. · 2017 · Allergen-specific immunoglobulin E and allergic rhinitis severity
- 12.Nickeisen JA, Georgitis J, Reisman RE. · 1986 · Lack of correlation between titers of serum allergen-specific IgE and symptoms in untreated patients with seasonal allergic rhinitis
- 13.Akdiş M. · 2009 · Immune tolerance in allergy
- 14.Çelebi Sözener Z, Mungan D, Cevhertas L et al. · 2020 · Tolerance mechanisms in allergen immunotherapy
- 15.Satitsuksanoa P, Angelina A, Palomares Ó et al. · 2022 · Mechanisms in AIT: Insights 2021
- 16.Schmidt-Weber CB, Blaser K. · 2005 · New insights into the mechanisms of allergen-specific immunotherapy
- 17.Nouri-Aria KT, Durham SR. · 2008 · Regulatory T cells and allergic disease
- 18.van Ree R, Hummelshoj L, Plantinga M et al. · 2014 · Allergic sensitization: host-immune factors
This article is general information about hayfever, not medical advice. It should not replace guidance from your GP, pharmacist or allergy specialist — particularly if you are pregnant, treating a child, or managing asthma alongside hayfever. Read our medical disclaimer.
