Trying to understand your question:
a. Can vaccination, by inducing antibodies, prevent infection, i.e. shield off the virus before it enters any cell, in locations that seem to be inaccessible for antibodies and lymphocytes?
b. If innate immunity successfully hinders infection and renders vaccination superfluous and redundant can the latter be considered effective?
c. Considering vaccination being able to prevent symptomatic or severe illness but not infectivity and epidemic spread what is the role of innate versus adaptive immunity in both, prevention of disease and epidemic spread?
If c. were correct understanding one prospective answer might be: Whereas, indeed, innate immunity prevents the spread of the virus, adaptive immunity prevents symptomatic disease. Another intricacy: In case innate immunity cannot prevent infection and epidemic spread, why doesn't vaccine/adaptive immunity come in stopping the spread - if it successfully prevents symptomatic disease? I see that point to your question and that's why I am out to publish my personal view, see inverted text at the end.
According to not very basic textbook knowledge antibodies/immunoglobulins are able to cross the blood tissue barrier. Immunoglobulins' sizes permit the evasion from blood and the invasion of interstitium/tissue/epithelia. IgE is a known example of specialized immunoglobulins that take care of outer epithelia. There do exist local lymphocytes, Langerhans cells, that make it across the vessel wall under regular circumstances, no inflammation or infection needed beforehand; they are in place.
In fact, not IgE, but IgA seems tailored for mucosa.
"IgA is the 2nd most common serum Ig. IgA is the major class of Ig in secretions - tears, saliva, colostrum, mucus. Since it is found in secretions secretory IgA is important in local (mucosal) immunity. Normally IgA does not fix complement, unless aggregated. IgA can bind(...) to some cells - PMN's and some lymphocytes."
While the question whether antibodies not only cross the blood-epithelial barrier but the blood-air-barrier as well is to be answered to the affirmative, there is a debate about the extent to which this holds for the fencing off of respiratory at the blood-air-barrier (not blood-tissue barrier), which makes your question non-trivial:
"...Translocation of large serum proteins (e.g., albumin, IgG) via paracellular routes by restricted passive diffusion does not appear to be the primary route, although under pathological conditions such passive diffusion may become the main route of protein leak." Protein transport across the lung epithelial barrier
As the quote above might suggstest the response of the adaptive immune system might seem late or reluctant, in accordance with the intention of your question I assume. Adaptive immunity might set in when infective spread has already happened. Even if antibodies have not waned they do not seem to be very willing to fit in where or when needed, in the mucosa.
On the other hand, imagine just one single epithelial cell the infection of which adaptive immunity could not prevent. If any shedding of virions from that one cell will encounter antibodies, and any lysis of that one cell will immunize local lymphocytes in between infected single cells of the epithelial you may consider vaccination/adaptive immunity effective.
Effectiveness of adaptive immunity may not being perturbed if it allows the transfection of one single cell as this signal of invasion is needed to trigger defence cascade.
Antibodies in between cells of epithelia and local lymphocytes, "Langerhans cells", may not be able to "prevent infection", however in principle, these elements of the adaptive immune response are able to prevent any further spreading.
Regarding the argument that there are no antibodies in the mucus, on the outside to prevent any "one cell" being invaded by virus one must admit that, in principle, this goes for the innate immune system as well as far as it is based on cell signaling, too.
In other words: adaptive immunity needs initiating infection to start a signaling cascade and does not prevent such infection; it would logically stop itself from starting. However, same applies to the interferon system of innate immune system that needs infection to start the interferon cascade.
*The following is my personal opinion that tries to answer your question "in deep".
"How can vaccines be effective against respiratory viruses when it is the innate immune system that is the primary response to such pathogens?"
Yes, you are right in some way. Indeed, there seem to be many variants or even species of respiratory viruses where vaccines are able to prevent symptomatic disease, however are not able to restrict viruses in replication sufficiently in order to prevent epidemic spread and non-symptomatic infection.
For instance, he Omicron variant of the Corona virus CoV-19, arguably a new serotype, may well illustrate a yet non-accepted principle of mutational viral evolution that pertains to balancing the innate and the adaptive immune system, assuming that the virus renders itself, paradoxically, more vulnerable to the innate system or other factors of the non-adaptive innate immunity, thereby not contacting the adaptive immune system and circumventing it, not even causing "much" immunity. This principle of escape from immunitiy is different from the strategy of hiding away by turning silent, especially by integrating, as retro viridae do, into the genome. My point is that from a single cell, compare the above, there might leak out into the air, lung a very large amount for infectious virus particle, so there is no latency at all. There is only a restriction by the innate immunity, that, in the intention of your question, is "just" not strong enough to stop infectivity and shedding of infectious virus by isolated cells.
Counterintuitively mutations turn out to be successful that render the virus less pathogenic and/or less infectious because the virus refrains from defending itself against the innate response as it is rewarded by non-immunizing and non-coping with existing adaptive immunity. It is the price the adaptive defence pays out to the virus for the virus weakening itself to a point of being beaten in first line by the innate immune system. In that mutational to and fro there are limits: for the virus there is a minimum of infectivity that must be "left over". Otherwise there will be some remake of the weakened.
Thus, vaccines may tend not to prevent the infectious spread. This is no trivial posting: the adaptive immune systeme accepts infectivity that is not pathogenic, not intrusive enough for to be bothered. The being late and the ineffectiveness is the price mutations certain respiratory viruses are being awarded if they let themselves be restricted to no invasiveness of the body, thus, in principle, harmlessness, paired with high incidental rates and epidemic spread. If there is hiding away of retro viruses, there is retreat of certain respiratory viruses.
The principle of evolution I hereby postulate thus pertains to the selective advantage for the virus that lies in not inducing immunity by not encountering antibodies and/or antigen presenting cells. Stated principle is that adaptive immunity, hence vaccination, by evolutionary art, does not fill the gap of infectiousness, epidemic infectivity, that innate immunity may or may not open.
It is the selective advantage viral evolution must have: the spread. Let me explain the spread. To spread is the reward adaptive immunity does not take away. Only then viral mutations find succes in letting the viruses being dampened, at the verge of extinction, by the interferon system of innate immnity. Thus vaccination, by principle, in many cases can only prevent disease, not infection.
Known mechanisms of adaptive immunity seen anew show that adaptive immunity "comes late":
Antigen presenting cells take up antigens that are derived from already infected, then succumbed, lysed cells.
T-cytotoxic cells await the apoptotic signal of already infected cells - most important, as an argument: specific T-Killer cells are known to become "anergic" when encountering their target, they have to wait until they get primed in lymph nodes, they come very late
The only defense of the adaptive system seems to be "neutralizing" antibodies that throw themselve in between the virus and the cell, theoretically. But then: they wane very quickly, and in my opinion, this regular waning fast of antibodies is coherent with the stated principle of reluctancy of the adaptive response.
What regards the viral turning itself either more or less exposed to the innate system of immunity I name two mechanisms, there may be more:
Respiratory Syncytial Virus by its name exemplifies: like Corona-Viridae this respiratory virus induces syncytialisation, i.e. fusion of one infected cell with others that surround it. While this is considered circumventing the adaptive immune system as far as more and more cells are infected without virus entering the interstitial or humoural space in between cells it is - in terms of my arguing - a mechanism of balancing and modulation: known are viral mutations that change binding of viral factors to syncytialization promoters of the host cell thus changing the degree of pushing back the entry of adaptive immune response.
As far as respiratory virus mentioned in your question use the way of syncytialization of infection one can say vaccines will be dampened. Vaccination sets in only as soon as there is lysis of syncytia (for the APS to uptake antigen, after "persistence ended" and/or MHC-presentation by syncytia with preexisting immunity).
Very intriguing in the context of your question is the barely popular fact of the placenta more or less being a syncytia that prevents the adaptive system of immunity from working, as it is said to block contacting the father's foreign antigens. Viral genes in the humane genome are held responsible. Analogy permitted, the pneumocytes type II, target cells of CoV, are very extended in form and appear as large extended shields. It is rare knowledge that CoV induces their syncytialisation, and if the latter is considered "infection", it is hidden and cannot be coped with by adaptive response nor vaccination. Thus, if induced by viral infection, syncytia of the lung cells can not only be seen as hideaways from the adaptive immune system but also as,in principle, fencing off a separate room - the mucosal room - which antibodies and lymphocytes cannot enter, which refers to your question.
[Liangyu Lin et al. 2021],14Syncytia formation during SARS-CoV-2 lung infection: a disastrous unity to eliminate lymphocytes
Cattin-Ortolá et al.https://pubmed.ncbi.nlm.nih.gov/34504087/
Sequences in the cytoplasmic tail of SARS-CoV-2 Spike facilitate expression at the cell surface and syncytia formation*
"Placental transfer - IgG is the only class of Ig that crosses the placenta. Transfer is mediated by a receptor on placental cells for the Fc region of IgG."
The Omikron variant of Cov might be an example of a presumably highly infectious, (in many cases) but non-symptomatic disease that still manages to cause the formation of antibodies. According to my reasoning and in the intention of your question I assume their building up might be weak, which, in result, has already be confirmed by re-infection with Omicron - within same season - being reported in Great Britan. Even if there were adapted vaccination against a respiratory virus variant, according to my reasoning, it should "not work well" against infectivity, non-pathgenicity only following suit the non-contacting of the realms of adaptive immunity, to affirmatively answer your question and putting my reasoning up for test in the near future, hopefully.
I will reference all this by tomorrow if allowed to.