Social Anxiety Disorder (SAD) is a condition characterised by intense fear of negative evaluation by others. Research suggests the disorder is relatively common, particularly during adolescence, which is the primary developmental period for onset for SAD (Merikangas & Avenevoli, 2002). When untreated, the disorder is unlikely to remit, often following a decades-long course in the majority of individuals who do not receive treatment (Keller, 2003). The disorder is highly comorbid with other psychiatric disorders (Beidel et al., 2007; Chartier et al., 2003), with evidence suggesting SAD predisposes the development of other conditions such as major depressive disorder (Cummings et al., 2014) and substance use disorder (Wittchen et al., 1999). Further, the disorder is associated with severe negative consequences across many life domains (Crawley et al., 2008; Mendlowicz & Stein, 2000; Olfson et al., 2000). However, the disorder is also difficult to treat. Individuals with SAD demonstrate poorer treatment response to generic anxiety treatment programs (Crawley et al., 2008; Scaini et al., 2016), highlighting the importance of addressing disorderspecific mechanisms in treatment, such as negative self-beliefs, attentional biases, post-event processing, safety behaviour use, and social skills deficits (Clark & Wells, 1995; Spence & Rapee, 2016). When treatments address these factors, individuals with SAD often achieve superior rates of remission compared to those in generic programs (Baer & Garland, 2005; Beidel et al., 2006; Herbert et al., 2008). However, a further compounding issue is that treatment access rates are very low in individuals with SAD, indicating the need for alternative modes of treatment that may address barriers to access (Burstein et al., 2011; Grant et al., 2005). Research aimed at identifying the central mechanisms of SAD is ongoing, and some potentially promising avenues, such as personality-informed perspectives, have received little attention by researchers (Kimbrel, 2008). The current program of research was designed to address these outstanding issues in the literature with a series of three empirical studies, presented as papers. The first paper describes a study that examined Spence and Rapee’s (2016) aetiological model of SAD. Although a promising model for the consolidation of the complex array of factors implicated in the development of SAD, this model had not been the subject of empirical testing. To examine the model, adolescents and emerging adults (N = 634, age range = 16 to 25 years, M age = 19.95 years, SD = 2.19) completed a survey measuring social anxiety and other variables implicated in SAD. Data were than analysed using structural equation modelling. Results showed that the proposed model accounted for 78% of the variance in social anxiety, and fit the data well after removing nonsignificant pathways and covariances. The indirect effects of genetic/temperamental and environmental factors on social anxiety, via behavioural and cognitive factors, were also examined and discussed. Altogether, Study 1 provided the first empirical evidence supporting the use of Spence and Rapee’s (2016) aetiological model in treatment and research on SAD. Following this, the second study examined the preliminary efficacy and acceptability of an intensive, group-based, disorder-specific cognitive behavioural therapy (CBT) intervention for adolescents with SAD, based on the Spence and Rapee (2016) model. An intensive program had, to date, not been investigated in adolescents with SAD. Fourteen Australian adolescents with SAD (78.6% female, M age = 13.93 years, SD = 1.14) and their parents completed the program, plus measures of treatment satisfaction, and provided feedback about positive and negative aspects of the program. Clinical diagnostic assessments and outcome measures were administered pre-treatment, post-treatment, and at 6-month follow-up. At post-treatment, 32.3% of participants no longer met criteria for SAD diagnosis, increasing to 42.9% at follow-up, and participants showed sizeable improvements in measures of symptoms and psychosocial functioning over time. Post-treatment satisfaction scores were very high for adolescents and parents. This study supported the potential value of intensive programs as a means of increasing treatment access in adolescents with SAD. Feedback from adolescents and parents for improving the program is discussed. Following from Study 1, Study 3 considered potential advances in conceptualisation of SAD by examining the potential utility a personality-based perspective. To do this, it tested Kimbrel’s (2008) model of the development and maintenance of SAD, which suggests that sensitivity in two neurobiologically-based personality systems, the behavioural inhibition system (BIS) and the fight-flight-freeze system (FFFS), are primary drivers of social anxiety. Participants were 392 undergraduate students (M age = 20.03 years; SD = 2.58; 294 females, 96 males) who completed a self-report survey battery. Sensitivity in BIS but not FFFS was found to mediate the relationship between childhood behavioural inhibition and social anxiety. This indirect effect was moderated by some environmental factors. Further, the relationship between BIS and social anxiety was mediated by several cognitive and behavioural factors, in line with Kimbrel’s model. These findings provided partial support for Kimbrel’s model, but suggested that BIS (rather than BIS and FFFS combined, as originally proposed in the model) is the primary determinant of social anxiety. BIS sensitivity as a personality trait appears to be associated with many of the beliefs, cognitive processes, and behaviours that maintain SAD, and warrants further investigation. In sum, the research conducted was concerned with providing evidence that may help to reduce the prevalence of SAD in the population. It provided the first direct evidence in support of Spence and Rapee’s (2016) model of SAD, and then applied this model in the development of an intensive treatment program for adolescents diagnosed with SAD. Finally, the research analysed Kimbrel’s (2008) model of SAD, suggesting revisions to the model, while also highlighting potentially promising avenues for further research.