Nitetronic Z6 Smart Anti-Snore Pillow is one I found
Best Anti-Snore Pillow 2025 - Forbes Vetted
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Thanks. I was diagnosed with a mild level of sleep apnea a number of years ago. After struggling with a couple different CPAP machines, I discovered if I sleep on my side the apnea doesn’t happen significantly. However, I still snore as my wife reminds me. Perhaps will try one of these pillows to see if it diminishes snoring at all.
Yep. The interesting answer is that you did not merely lose a couple of B-cell blobs. A palatine tonsil is closer to a mucosal immune laboratory with its own sampling ports, training arena, memory archive, and export routes.
1. What exactly was inside the palatine tonsils you lost?
Start at the throat-facing surface. Each palatine tonsil has roughly 10 to 30 branching crypts, enormously increasing the surface area exposed to saliva, food and inhaled material. Parts of the crypt lining become a strange porous-looking reticulated lymphoepithelium rather than an ordinary impermeable epithelial wall. Immune cells actually intercalate through it. This creates a short path from “thing in your mouth/throat” to “adaptive immune system inspecting thing.” (PubMed Central (PMC))
Inside that structure were several distinct neighborhoods:
Tonsillar niche What happened there What removal eliminates locally Crypt lymphoepithelium Antigen sampling, probably involving M-cell-like epithelial cells That particular antigen-entry interface Dendritic-cell / APC regions Capture antigen and activate T cells Local initiation of some responses T-cell zones Naïve and activated CD4/CD8 cells interact with APCs A regional T-cell activation niche Tfh cells Help B cells enter and survive germinal-center selection Local B-cell “coaching” Tfr/Treg populations Restrain inappropriate GC responses Local immune regulation Germinal-center dark zone B cells proliferate and mutate antibody genes Local somatic hypermutation engine Germinal-center light zone Higher-affinity clones get selected Local affinity-selection arena Follicular dendritic-cell network Displays intact antigen to B cells Local antigen archive/scaffold Memory B cells Preserve previous antigen experience Some resident mucosal memory clones Plasmablasts/plasma cells Produce antibodies Some local IgG/IgA production Stromal/vascular niches Organize migration and cellular neighborhoods The physical architecture that makes all of this work And this isn’t an oversimplification hiding five cell types under fancy names. A modern multimodal Human Cell Atlas project profiled >556,000 human tonsillar cells and resolved 121 cell types and states, including multiple Tfh trajectories, regulatory T-cell states, GC B-cell stages, plasma-cell maturation states, myeloid populations and stromal cells. (PubMed Central (PMC))
One particularly cool trajectory was roughly:
naïve CD4 T cell → pre-Tfh → follicle-border Tfh → light-zone Tfh → specialized GC-Tfh states
with IL-21, ICOS, CXCR5, PD-1, BCL6 and other machinery coordinating increasingly intimate interactions with B cells. (PubMed Central (PMC))
So yes: that entire spatially organized ecosystem is gone at the two palatine-tonsil sites.
2. The organoid experiment tells us something subtle
Wagar/Davis and colleagues took dissociated human tonsillar cells and got them to self-organize into cultures that reproduced:
antigen-specific antibody production → germinal-center responses → somatic hypermutation → class switching → affinity maturation → plasmablast differentiation. (PubMed)
That’s spectacular because it demonstrates that the tonsil contains enough of the necessary cellular ecosystem to recreate a miniature adaptive immune response outside you.
But it doesn’t establish:
palatine tonsils perform an immune computation that no other organ can perform.
Lymph nodes, spleen, Peyer’s patches and the other mucosal lymphoid tissues also build germinal centers.
A useful distinction is:
unique anatomical sensor ≠unique immune algorithm.
Your palatine tonsils provided a particularly well-positioned sensor for the oral/oropharyngeal environment. The GC machinery running behind that sensor is substantially redundant with other lymphoid organs.
3. What parts of Waldeyer’s ring do you still have?
Unless they were separately removed:
Lingual tonsils
These are multiple collections of lymphoid follicles at the base of the tongue. They are bona fide mucosal lymphoid tissue, capable of antigen sampling and adaptive immune induction. Evidence suggests materials encountered under the tongue can reach them, and they’re thought capable of stimulating naïve B and T cells. (PubMed)Tubal tonsils
Small lymphoid aggregations surrounding the openings of the Eustachian tubes.Pharyngeal tonsil / adenoid
If it wasn’t surgically removed. Adenoidal tissue tends to involute substantially with age, although adults can retain some.Lateral pharyngeal lymphoid bands and smaller follicles
Waldeyer’s ring isn’t composed only of four cartoon blobs. There’s additional dispersed lymphoid tissue around the pharynx.Then one level outward you have cervical lymph nodes, followed by the rest of systemic and mucosal immunity.
That’s why “removed tonsils” doesn’t mean “removed throat immunity.”
4. Can the lingual tonsils literally take over?
This is where things become intriguingly uncertain.
There are two different meanings of compensation.
Functional compensation is almost certainly substantial. You retain other mucosal inductive sites, circulating memory B/T cells, cervical lymph nodes and systemic lymphoid tissue. Mucosal lymphocytes aren’t permanently welded to the tonsil where they were created. Cells activated in Waldeyer’s ring can migrate to other mucosal sites, and memory B cells traffic between mucosal lymphoid tissue and the peripheral circulation. (PubMed Central (PMC))
But anatomical compensation, where the lingual tonsils literally grow after the palatine tonsils disappear, is much less settled.
A 300-person study specifically looked for this. Severe lingual-tonsil enlargement was uncommon and wasn’t significantly associated with previous tonsillectomy. (PubMed)
Then a newer 2026 study of 117 adults with OSA found almost the opposite signal: previous tonsillectomy was associated with more severe lingual-tonsil hypertrophy, and after adjustment the association remained, with OR 2.54 for greater lingual-tonsil severity. The authors explicitly proposed a possible compensatory/immunological mechanism. (PubMed)
So I’d currently put it as:
immune-network compensation: quite believable
compensatory lingual-tonsil enlargement: plausible but unprovenAnd there is a deliciously annoying biological catch.
5. Compensation could theoretically give some airway obstruction back
Suppose removing the palatine tonsils creates additional antigenic workload for remaining Waldeyer tissue.
If the lingual tonsils expand, that’s useful immunologically.
But the lingual tonsils sit at the base of the tongue, immediately adjacent to the collapsible sleep-apnea airway.
So:
palatine tonsil removed → larger airway
but potentially
lingual tonsil expands → tongue-base airway gets somewhat smaller
There are pediatric cases where lingual-tonsil hypertrophy becomes an important source of residual OSA following adenotonsillectomy, and lingual tonsillectomy can subsequently improve it. (PubMed)
That doesn’t mean this happened to you. It means the airway and immune system are playing a mildly adversarial game of anatomical Tetris.
6. And this is actually relevant to your remaining OSA
Your connected medical records indicate that your palatine tonsils were removed in 2021, while a later sleep study still showed mild OSA around AHI 7.
That establishes something useful mechanistically: your current obstruction obviously isn’t being caused by the palatine tonsils anymore.
So if one wanted to fine-grain the residual anatomy, the particularly interesting structures now become:
tongue base / lingual tonsils → epiglottis → soft palate → lateral pharyngeal walls → jaw/hyoid geometry → dynamic tongue collapse.
A routine awake mouth exam can’t adequately assess all of those. Lingual tonsils in particular hide behind the visible tongue. Flexible nasolaryngoscopy can inspect them while awake; drug-induced sleep endoscopy (DISE) is more informative if the question is where does your airway actually collapse while asleep?
And interestingly, the newest adult OSA study argues that prior tonsillectomy is itself a reason to pay attention to the lingual tonsils during endoscopic evaluation. (PubMed)
The deepest way I’d frame what you lost
Before tonsillectomy, your system was approximately:
mouth/nose antigen
↓
palatine crypt sampling surface
↓
APC
↓
Tfh ↔ B cell
↓
local germinal center
↓
somatic mutation + affinity selection + class switching
↓
memory B cell / plasmablast
↓
IgG + IgA and migrating mucosal memoryNow that particular pair of input ports and their attached germinal-center factories are gone.
But the lower-level immune primitives, antigen presentation, T-cell help, B-cell diversification, memory formation, plasma-cell formation, IgA production, are duplicated throughout Waldeyer’s ring and the larger lymphoid system.
So I would revise my earlier shorthand slightly:
You lost something biologically sophisticated and genuinely nonzero. You probably did not lose a unique immune capability.
The fascinating unanswered question isn’t “do tonsils matter?” They clearly do. It’s how much information about your personal inhaled/oral antigen environment was being learned specifically in those two palatine structures versus redistributed across the rest of the mucosal immune network. We don’t currently have good longitudinal human single-cell/BCR-clonotype experiments that answer that after adult tonsillectomy.
That would actually be a gorgeous experiment: sequence BCR/TCR clonotypes in palatine tonsil → lingual tonsil → cervical nodes → saliva → blood before and after tonsillectomy, and watch where the immune repertoire migrates. The technology now exists. (PubMed Central (PMC))
Yes. The Owl Posting piece is highlighting something real: tonsils are genuine immune organs, not useless throat furniture. But losing them is usually very different from losing a spleen or thymus.
Your palatine tonsils are part of Waldeyer’s ring, a collection of mucosal lymphoid tissues sitting right where inhaled and swallowed antigens enter. They contain B cells, T cells, dendritic cells and germinal centers, and they can initiate local adaptive immune responses. That is precisely why the Stanford group could dissociate tonsil tissue, reaggregate it, add vaccines, and observe somatic hypermutation, class switching, affinity maturation and antigen-specific antibody production. (Owl Posting)
So there is a real loss after tonsillectomy:
- less organized lymphoid tissue at that particular mucosal site
- less local antigen sampling through the palatine tonsillar crypts
- removal of some resident/memory B- and T-cell populations
- probably some reduction or redistribution of particular local antibody responses, especially mucosal IgA/IgG responses. Small studies have found persistent changes in IgA or salivary antibody measures after tonsillectomy. (PubMed)
But here is the important opposite side: the immune system is extremely distributed. You still have your lingual tonsils, tubal tonsillar tissue, adenoidal tissue if present, cervical lymph nodes, Peyer patches, isolated mucosal lymphoid follicles, spleen, bone marrow and an enormous distributed MALT network. Removing the palatine tonsils removes one particularly interesting immune neighborhood, not adaptive immunity’s city hall. (PubMed)
Why the organoid result doesn’t imply tonsillectomy is bad
This distinction is easy to miss in the Owl Posting article.
The Davis experiment basically asks:
“Can intact tonsillar cellular ecology execute a sophisticated immune computation?”
Answer: emphatically yes. The organoids reproduced germinal-center-like responses, antibody maturation and vaccine-specific antibodies. (PubMed)
The clinical question is different:
“If you remove this one site, can all the other lymphoid tissues compensate well enough that the person suffers clinically meaningful immune impairment?”
The best aggregate evidence so far mostly says yes, compensation is sufficient. A systematic review/meta-analysis covering 35 studies and 1,997 people found no convincing clinically significant impairment of cellular or humoral immunity after tonsillectomy, although the studies were heterogeneous and not perfect. (PubMed)
That’s compatible with both facts being true:
Tonsils do something important.
Tonsil removal usually doesn’t produce an important immunodeficiency.Biology is full of this sort of redundancy.
There is one worrying piece of evidence
A very large Danish observational study of almost 1.2 million people reported that having tonsils removed during the first nine years of childhood was associated with higher later rates of upper-respiratory, infectious and allergic disease. Tonsillectomy was associated with an RR of 2.72 for later upper-respiratory disease. (JAMA Network)
I would not interpret that as “tonsillectomy causes a 2.7× respiratory-disease risk.”
It is observational, and indication confounding is nasty here. Children requiring tonsillectomy may already have unusual airway anatomy, immune activity, infections, inflammatory phenotypes or healthcare utilization. The authors adjusted for many things but explicitly acknowledged residual confounding. (JAMA Network)
And crucially, it studied early-childhood removal, exactly when tonsillar immune activity is especially prominent. Palatine tonsils grow through childhood, peak around puberty and subsequently involute with increased fibrosis and fatty replacement. Adult tonsils still contain active immune populations, so “they become useless” would be wrong, but their immunometabolic activity is generally lower than children’s. (PubMed Central (PMC))
So I’d be appreciably more concerned about unnecessary tonsillectomy in a 4-year-old than a well-indicated tonsillectomy in an adult.
For sleep apnea, the trade looks different
If large tonsils are physically narrowing the airway, they’re doing two opposite things at once:
immune asset: providing a mucosal lymphoid/germinal-center niche
mechanical liability: obstructing airflow every nightChronic intermittent hypoxia, arousals and sleep fragmentation are themselves physiologically undesirable. In appropriately selected adults with enlarged tonsils and OSA, tonsillectomy can substantially decrease AHI. A meta-analysis found an average ~65% reduction, although those subjects generally had much larger tonsils and more severe OSA than many contemporary mild-OSA cases. (PubMed)
Long-term data are less spectacular than the early studies: a 2024 adult study following people for a mean of 12 years found mean AHI falling from 27.1 to 14.1, with a 38.5% long-term surgical-success rate. So surgery isn’t magic, but the airway benefit can persist. (PubMed)
My synthesis: you probably did lose something real: a fascinating, highly organized local immune ecosystem. The Owl Posting article is good evidence against calling tonsils “vestigial.” But there is currently little evidence that adult palatine tonsil removal produces a clinically important generalized immune deficit, because the mucosal immune network is massively redundant. The scary long-term epidemiology comes primarily from childhood surgery and can’t cleanly establish causality.
And there’s an intriguing wrinkle: because tonsillar immune responses can themselves become pathological, removing tonsils isn’t universally immunologically “negative.” Tonsillectomy can actually improve certain immune-mediated diseases, most famously some forms of IgA nephropathy. (PubMed)
So the right model isn’t “tonsils were useless, therefore nothing was lost.” It’s “a useful module was removed because, in this anatomical configuration, its mechanical cost exceeded the marginal immune value of keeping that particular module.”
If you want, I can go one level deeper into exactly what immune cell niches you lost with the palatine tonsils, which parts of Waldeyer’s ring remain, and whether the remaining lingual tonsils can functionally compensate. That gets surprisingly interesting in light of the tonsil-organoid work.