To answer the bounty question
I am looking for a simple and straightforward answer which describes in a few sentences the mechanism by which the adaptive immune system, informed by a vaccine, would prevent infection of the epithelia of the respiratory system by a virus.
a (not the) mechanism by which the adaptive immune system affects respiratory viruses before cell entry is antibodies presence in mucus, which does seem to have a noticeable [counter]effect on viral particle mobility in mucus for the specific viruses against which the host has antibodies. (See last section of this answer for details.)
However, I'll also that (adaptive) humoral immune system response in the mucus is hardly the end of the adaptive immune system relevance to the epithelium, as avoiding cellular infection altogether cannot be guaranteed by mucus (even with antibodies in it). The epithelium is also "guarded" by adaptive cellular mechanisms (e.g. T cells) that preferentially attack [epithelium] cells infected with specific viruses, as "bits" of these viruses are exposed on infected cells' surface via MHC I.
Basically, the immune system does function in the respiratory epithelium contra to your theory, and the usual cascade of innate mechanisms triggering the adaptive ones also works in the epithelium:
Several immune cell populations are resident in epithelium including CD103+ CD8+ T cells and CD103+ conventional dendritic cell populations which act as sentinel cells. Other immune cell populations including innate lymphoid cells (ILCs), mucosal associated invariant T cell (MAIT), natural killer cells (NKT) and γδ T cells are in close proximity to the epithelium. [...]
The airway epithelium utilizes structural and barrier defence provided by the mucociliary escalator and their incumbent anti-microbial proteins, and intra- or epithelial-associated immune cells like resident dendritic cells, invariant natural killer T (iNKT) cells, γδ T cells and intra-epithelial lymphocytes.
You're correct that respiratory viruses often have the epithelium as their preferred/evolved target, but this is also where they are usually "defeated" (in fact if they're not defeated there, the host is usually in big trouble). Furthermore, experimentally interfering with this signalling cascade results in much worse outcomes--see emphasized part on dendritic cells further below.
Upon binding sialic acid receptors on the epithelial cell surface, IAV are internalised via receptor-mediated endocytosis [...] The host cell begins sensing IAV as soon as it is internalised, utilising pathogen recognition receptors (PRRs), primarily the Toll-like receptors (TLRs) and RNA-sensing RIG-I–like receptors (RLRs), such as retinoic acid–inducible gene I (RIG-I) and melanoma differentiation-associated protein 5 (MDA-5) [...]
Those (TLRs, RLRs etc.) are indeed part of the innate immune system, but that's not the end of the story:
Activation of type I interferons is the key consequence of intracellular recognition of IAV infection by TLRs and RLRs. These cytokines bind to the IFN-α/β receptor (IFNAR) on infected as well as neighbouring cells and induces the transcription of a large group of genes (interferon stimulated genes or ISG) whose main task is to limit spread of infection. [...] In epithelial cells, type I IFN has the additional task of acting as an early warning system, communicating viral threat between infected and uninfected cells. [...]
But epithelial cells also signal "the invasion" through a more specific mechanism: type III interferons (IFN-λ). In any case:
Activation of both type I and III IFN results in induction of hundreds of ISGs. ISGs trigger apoptosis, shut down protein synthesis and activate key components of the innate and adaptive immune systems, including antigen presentation and production of cytokines involved in activation of T, B, and natural killer (NK) cells.
So, thanks to interferons the adaptive immune system does get triggered, even in the epithelium. Furthermore
There is substantial cross-talk between epithelial and immune cells sequestered in the epithelium. CD103+cDCs continuously sample the airway via extended dendrites and respond to chemokines and cytokines (including type I and III IFNs) and DAMPs secreted by IAV- infected epithelial cells
Intra-epithelial dendritic cells are essential to generate protective IAV-specific CD8+ T cells; mice lacking this DC subset succumb to severe disease and impaired viral clearance.
Basically, not having the adaptive immune system active/functional in the epithelium is usually fatal for the host, even in relation to "mere" influenza infection. DCs "act as messengers between the innate and the adaptive immune systems."
Also, at least the epithelium of the lungs has additional defenses (iNKT cells). If you look at their Wikipedia page, the NKT cells are somewhat of a hybrid of adaptive (T cells) and innate (NK cells) immune system; they in turn release a plethora of signalling molecules "large quantities of interferon gamma, IL-4, and granulocyte-macrophage colony-stimulating factor, as well as multiple other cytokines and chemokines (such as IL-2, IL-13, IL-17, IL-21, and TNF-alpha)" that activate the adaptive immune system, although I think NKTs mostly respond to bacterial rather than viral infections. (I could be wrong though on this.) But if they do "get triggered", e.g. in a co-infection scenario (not uncommon in pneumonias), NKTs seem to help with the viral [part of the] infection as well (going back to quoting from the review paper [1st link]):
In the mouse, presence, and exogenous activation, of lung iNKT cells by α-GalCer, protects against lethal H1N1 and H3N2 influenza in prophylactic settings.
But to reiterate again the more common mechanisms:
The epithelial cells’ attempt to clear IAV results in inevitable tissue injury, in part because of collateral damage from the accompanying innate immune response and direct induction of apoptosis by IAV, but also because cytotoxic T cells will eventually kill cells with IAV peptides presented on their MHC class I molecules. If epithelial cells are not killed they undergo apoptosis or de-differentiation. If IAV reaches the alveolar epithelium, various injurious events can occur. [...]
Speaking of that last (emphasized) issue, the influenza viruses "try pretty hard" to make themselves invisible to the MHC I pathway.
we showed that infection of several cell types, including epithelial A549 cells, with a panel of IAV and IBV viruses downregulated the surface MHC-I expression on IAV/IBV-infected cells during the late stages of influenza virus infection in vitro. [...] Importantly, the two viruses utilized two distinct mechanisms for MHC-I downregulation.
If MHC I (triggering T cells) wasn't a problem for them, why would they have evolved these camouflage/countermeasures?
Since you confusion (or argument) seems to be whether Cytotoxic CD8+ T cells are or aren't part of the adaptive immune system (they are), let's side-step such categorization discussion and simply observe that a Covid-19 mRNA vaccine trains them so that significant fraction recognize the virus bits:
Fractions of RBD-specific IFNγ+ CD8+ T cells reached up to several per cent of total peripheral blood CD8+ T cells in immunized individuals
RBD here means the receptor binding domain (protein) of the specific virus (SARS-CoV-2 in this case).
(The same is true for vaccines that target the full spike protein, which are the ones actually approved by regulators, although the corresponding paper(s) still seem to be in the preprint stage. The latter paper speaks of "S-specific CD8+", meaning SARS-CoV-2 spike-specific.)
Now, if you want to focus/ask only what happens before any cell entry, the humoral immune system is present in mucus. It (also) has innate (e.g. mucins, lactoferrin) and adaptive components; antibodies are present in the mucus.
Antibodies importance (relative to innate mechanism) in mucus has been less studied, but their presence in mucus has surely been (commonly) observed, and some studies comparing viral movement speeds in mucus do suggest that specific antibodies slow down the corresponding viruses in mucus e.g.:
To investigate whether trapping of influenza in airway mucus can be attributed primarily to haemagglutinin binding to mucin-associated sialic acid, we prepared VLPs fluorescently labelled internally using HIV-1 GAG-mCherry capsid proteins in the core, and expressing both neuraminidase and haemagglutinin from H1N1 (influenza A/PR/8/34) (WT-Inf), or the same neuraminidase and haemagglutinin that has the sialic acid-binding domain deleted (ΔSAB-Inf) and hence cannot bind directly to mucins. Interestingly, both WT-Inf and ΔSAB-Inf were trapped in airway mucus to a similar extent as H1N1 and H3N2, with roughly 98% of WT-Inf and 97% of ΔSAB-Inf immobilised in airway mucus and average diffusivities ∼1700- and ∼1100-fold lower than expected speeds in buffer, respectively (figure 1b, online supplementary movies S4 and S5). [...]
Using whole-virus ELISA assays, we detected substantial quantities of endogenous IgG and IgA against influenza in airway mucus (data not shown), as well as against both WT-Inf and ΔSAB-Inf VLPs. [...] This leaves open the possibility that influenza-specific antibodies in airway mucus may immobilise virions by cross-linking the antibody–virus complex to mucus constituents, such as mucins. We sought to measure virus and VLP mobility in airway mucus devoid of antibodies; however, we were not able to adequately remove Ig by dialysis, possibly due to membrane clogging, and mucus secretions isolated from air–liquid interface cultures of bronchial epithelial cells did not produce a sufficiently rigid matrix to immobilise mucoadhesive latex nanoparticles. We also attempted to “saturate” the mucus–antibody barrier by mixing >20-fold more unlabelled than labelled influenza viruses into airway mucus prior to adding labelled viruses, and still observed no discernible difference in the trapping of the labelled influenza viruses. Therefore, we investigated whether the lack of binding antibodies in mucus correlates to greater virus mobility by tracking HIV VLPs that were prepared similarly to the influenza VLP, but expressing HIV YU2 gp160. We found no detectable HIV-binding IgG or IgA in airway mucus (figure 1d, e), and HIV VLPs exhibited markedly greater diffusivity in airway mucus (figure 1b, online supplementary movie S6; p<0.05), with >45% of HIV VLPs classified as mobile and ∼10-fold higher ensemble effective diffusity than WT-Inf and ΔSAB-Inf. HIV VLP mobility was similar to that of PS-PEG in the same airway mucus samples (data not shown).
Together, these results demonstrate that influenza virus can be trapped in human airway mucus without binding to sialic acids on mucins, in good agreement with the evidence that human influenza viruses possess haemagglutinin that preferentially binds α2,6-linked sialic acids on the airway epithelium rather than α2,3-linked sialic acids on mucins. Trapping of influenza in human airway mucus can probably be attributed to the presence of influenza-binding antibodies that can cross-link individual virions to the mucus mesh network. Importantly, adhesive interactions between the array of pathogen-bound antibodies and mucus gel provide a universal strategy that enables the otherwise relatively nonadaptive and nonspecific biochemistry and microstructure of mucus secretions across different mucosal surfaces to be fortified with adaptive antibodies against an ever-changing spectrum of pathogens.
But before you get too excited about this finding, remember that the immune systems is "defense in depth", some virus particles will make it through the mucus, even if you do have specific antibodies against them there; this is when
the cellular mechanisms kick in. There's no one mechanism that is going to be 100% foolproof.