Yes, the exact mechanism for acclimization is still poorly understood; however, it has been demonstrated both in the field (technical and military) and research studies (some of which Gene posted earlier). Whether this is due to a decrease in bubble formation from possible reduction of gas nuclei or endothelial effects, or a decrease in response to bubbles present through a pathophysiological effect (or both?) has yet to be determined.
One idea that has been (and is currently being) studied is that there could be an inflammatory or immune adaptive response to prior exposure. Gene has already posted one of the references focused on chronic hyperbaric exposure effects on inflammatory mediators (Erssson et al). This study saw an overall rise of proinflammatory mediators after daily hyperbaric exposure for a month. However, they also saw a rise in anti-inflammatory mediators, suggesting the maintenance of an overall inflammatory system homeostasis. Their thought was this provides a certain protective mechanism unless the level of insult reached a 'threshold' and tipped the balance, possibly leading to DCS.
In regards to immune response, the Navy did a study where they saw a reduction in DCS (55% to 24%) in rats injected with a foreign protein:
Lower decompression sickness in rats by intravenous injection of a foreign protein. Undersea and Hyperb Med Soc 1997.
Their thought was the prior exposure to the foreign protein elicited an immune response, which lessened the subsequent immune response following the decompresson profile, and that this could possibly applied as a mechanism in diving adaptation (with the bubbles being the foreign object).
There are two other 'major' areas currently being studied in regards to acclimization mechanisms. One is nitric oxide (as mentioned previously in this thread), and the other is heat shock protein response. There have been a number of studies done in regards to nitric oxide production (and changes in endothelial function) and diving (Gene? :blinking

. Alf Brubakk's group in Norway has been the major contributor to research on nitric oxide and decompression (including exercise effects). I would recommend reading this paper for a better understanding:
Wisloff et al. Exercise and nitric oxide prevent bubble formation: a novel aproach to the prevention of decompression sickness? J Physiol. March 15 2004. 555(3): 825-829.
As for heat shock protein response, the Discussion section in Blatteau's recent paper does a nice job summarizing current work done on the idea:
Blatteau JE, Gempp E, et al. Predive sauna and venous gas bubbles upon decompression from 400kPa. Aviat Space Environ Med 2008. 79(12): 1100-5.
(As a side note with this paper, please don't jump in a sauna before your next dive! Remember these conditions are experimental and the results should not be interpreted in any way that will change your diving practice)
Heat shock proteins play a number of pivotal roles including acting as molecular chaperones (helping properly fold proteins and keep proteins from aggregating) and maintaining the intracellular environment. They are known to upregulate in response to stress (inflammation, infection, hypoxia, cold, heat, exercise to name a few). There are a couple of studies discussed in this paper, most of which point to some (but questionably signficant) protection of heat exposure prior to animal diving studies. One thing to point out is heat shock proteins are intricately weaved amongst a number of intertwined pathways (eg. inflammation, complement, nitric oxide)...so in addition to so many other questions, we would like to know how/when/where these proteins play a role in hyperbaric exposure, decompression sickness, and acclimization.
Have a great weekend, and please feel free to PM me if you are looking for additional references on this topic.
Dawn
PS - I tried to post links to all of these but since I am a newbie here I couldn't. Sorry! Just go to Rubicon for the Kayar paper and pubmed for Wisloff and Blatteau.