Seasonal IgE Surge in Birch Allergy Driven by IgE⁺ Plasmablasts: Q&A With Investigators

A new study identified IgE⁺ plasmablasts as the dominant drivers of seasonal IgE boosts in birch pollen allergy.

The cellular mechanisms driving seasonal surges in allergen-specific IgE have not been well defined. Therefore, investigators examined the role of plasmablasts in mediating these increases during pollen exposure.

Using longitudinal sampling across pollen seasons, epitope mapping, basophil activation assays, and IgE VH sequencing, the team found that when patients are naturally exposed to birch pollen, they produce more IgE antibodies from plasmablasts that target the Bet v 1 allergen. This increase happens without a similar rise in IgG antibodies. The findings clarify how effector cells are reloaded with allergen-specific IgE during seasonal exposure and position IgE⁺ plasmablasts as a potential therapeutic target in allergic disease.

The study showed that bet v 1–specific IgE levels increased significantly during peak pollen exposure compared with pre-season measurements (TP1 vs TP3; P <.01) and declined again after the season (TP3 vs TP5; P < 0.05). In contrast, bet v 1–specific IgG1 and IgG4 levels did not show significant seasonal changes, indicating that the IgE boost occurred without a synchronized IgG response.

In several individual patients, IgE kinetics were completely dissociated from IgG1 and IgG4 trajectories. Flow cytometry demonstrated a significant increase in circulating IgE⁺ plasmablasts (CD19⁺CD27⁺CD38⁺CD20low) during the pollen season, supporting their role as the primary source of secondary IgE production.

In this Q&A, investigators Maria Byazrova and Rudolf Valenta, both from the Federal Medical Biological Agency of Russia (FMBA Russia), discussed the study’s key insights, how these findings challenged the assumption that memory B cells drive IGE recall responses, and how these results helped explain why patients often experience worsening allergic symptoms with repeated seasonal exposure.

HCPLive: What is the key new insight this study provides about the cellular source of seasonal increases in allergen-specific IgE?

Byazrova: Plasmablasts are one of the main cells [that] are part of the secondary IgE-induced response. In this case, plasmablasts, which are one of the subset[s] of the B cells… [are] temporary [and] arise in the bloodstream after the high allergen exposure. They are producing secondary IgE, which can reward effector cells [and]

can induce allergic reactions. The plasmablasts are [an] extremely important subpopulation if we are talking about allergy development

Valenta: IG antibodies here have an unusually very short half-life, so usually it's about 3 days. So, if you start to develop IG antibodies when you are born here, you [can] become allergic. The thing is that CIG antibodies, if they [were] only in the circulation, would disappear very quickly, but they can bind to the receptors on the inflammatory cells, like… muscles and basophils. These cells can bind [to] the IG for a prolonged period, but the cells must be reloaded so that the person has an allergic reaction after a while.

HCPLive: How do your findings challenge the assumption that memory B cells or secondary class switching drive IGE recall responses?

Valenta: I think one of the strengths in our paper [was that] we showed that IG antibodies recognize different epitopes than IgG, and we analyzed the secondary antibody response with…the wild type [of] allergen that is folded and with fragments. Fragments worked with IgG, but not with IG. So, we can differentiate that there is no IgG boost, because we do not see that when we analyze with the broken parts of the antigen, the sequential epitopes.

HCPLive: How did these results help explain why patients often experience worsening allergic symptoms with repeated seasonal exposure?

Byazrova: When we have the birch pollen season, B cells activate, and they differentiate into the IGE plasmablast with [the] help of T cells. After this, this plasma blast circulates, which is literally activated B cells; they are producing IGE. This increase[s] the sensitivity of the patient during the birch pollen season because this additional IG can arm the effective cells.

HCPLive: what does the reloading of basophils with allergen specific IGE after seasonal exposure reveal about the timing and reversibility of allergic sensitivity?

Valenta: It's the same with the mast cells. They quickly reload. It's a kind of cycle when you watch it. For example, seasonal allergy, when the person is out of the season without allergen exposure, the IG [levels] start to drop down and so does with a little bit of a time shift.

In principle, if you put a person, let's say, for a year or two here to a different place where there [are] no birch trees, the sensitivity will drop further down. That means that you need to reload all the time, again and again, to maintain this sensitivity

References

Byazrova, M., Litovkina, A., Eckl-Dorna, J. et al. Seasonal allergen exposure recalls IgE+ plasmablasts to reload allergic effector cells. Immun. Inflamm. 2, 2 (2026). https://doi.org/10.1007/s44466-025-00018-w