Implicit self-esteem and narcissism: rethinking the link

Several studies have found that explicit and implicit self-esteem interact to predict narcissism. These findings have been interpreted as supporting the hypothesis that narcissists have high but fragile self-esteem. However, we contend that these findings are neither empirically consistent nor conceptually coherent. We instead hypothesize that explicit and implicit self-esteem should predict narcissism independently, respectively in a positive and negative direction. In a large multi-session study, we examined the interrelationships between narcissism, explicit self-esteem, and three indices of implicit self-esteem (showing good psychometric properties and some convergent validity). No evidence emerged that explicit and implicit self-esteem interacted to predict narcissism. However, as predicted, two measures of implicit self-esteem were inversely related to narcissism. Potential explanations for divergent findings are considered

Inclusion of theory-relevant moderators yield the same conclusions as Sedikides, Gaertner, and Vevea (2005): A meta-analytical reply to Heine, Kitayama, and Hamamura (2007)

Heine, Kitayama and Hamamura (2007) attributed the Sedikides, Gaertner and Vevea (2005) findings to the exclusion of six papers. We report a meta-analysis that includes those six papers. The Heine et al. conclusions are faulty, because of a misspecified meta-analysis that failed to consider two moderators central to the theory. First, some of their effect sizes originated from studies that did not empirically validate comparison dimensions. Inclusion of this moderator evidences pancultural self-enhancement: Westerners enhance more strongly on individualistic dimensions, Easterners on collectivistic dimensions. Second, some of their effect sizes were irrelevant to whether enhancement is correlated with dimension importance. Inclusion of this moderator evidences pancultural self-enhancement: Both Westerners and Easterners enhance on personally important dimensions. The Sedikides et al. conclusions are valid: Tactical self-enhancement is pancultural

Individual differences in self-enhancement and self-protection strategies: an integrative analysis

Research has identified a large number of strategies that people use to self-enhance or self-protect. We aimed for an empirical integration of these strategies. Two studies used self-report items to assess all commonly recognized self-enhancement or self-protection strategies. In Study 1 (N = 345), exploratory factor analysis identified four reliable factors. In Study 2 (N = 416), this model was validated using confirmatory factor analysis. The factors related differentially to the key personality variables of regulatory focus, self-esteem, and narcissism. Expanding this integrative approach in the future can reveal a great deal about the structure and dynamics of self-enhancement and self-protection motivation

The why's the limit: curtailing self-enhancement with explanatory introspection

Self-enhancement is linked to psychological gains (e.g., subjective well-being, persistence in adversity) but also to intrapersonal and interpersonal costs (e.g., excessive risk taking, antisocial behavior). Thus, constraints on self-enhancement may sometimes afford intrapersonal and interpersonal advantages. We tested whether explanatory introspection (i.e., generating reasons for why one might or might not possess personality traits) constitutes one such constraint. Experiment 1 demonstrated that explanatory introspection curtails self-enhancement. Experiment 2 clarified that the underlying mechanism must (a) involve explanatory questioning rather than descriptive imagining, (b) invoke the self rather than another person, and (c) feature written expression rather than unaided contemplation. Finally, Experiment 3 obtained evidence that an increase in uncertainty about oneself mediates the effect

Characterisation of T cell responses to proteins expressed during Human Cytomegalovirus latency

Human cytomegalovirus (HCMV) is a betaherpesvirus that establishes a lifelong infection in hosts. In the majority of cases, the immune response to primary HCMV infection limits viral replication and dissemination, such that overt clinical disease is prevented. However, the immune system cannot prevent the virus establishing a latent infection, which enables lifelong persistence. Historically, a long-standing view was that viral gene expression during latency was largely absent, thus facilitating the avoidance of immune detection. However, it has now been established that viral activity in latency is far from quiescent, and the expression of a number of viral genes is known to occur. Therefore, an important question arises: are T cells specific to these proteins generated, and, if so, why are HCMV latently infected cells maintained in the face of these potential T cell responses? Previous work has shown that two such viral gene products, UL138 and LUNA, are recognised by CD4+ T cells, with a subpopulation of these cells secreting the immunosuppressive cytokines interleukin (IL)-10 and transforming growth factor beta ($\beta$). However, little is known about the host immune response to other key latency-associated viral proteins; US28, UL111A, and UL144. Using overlapping peptide pools designed to cover the whole of the predicted amino acid sequence of these HCMV proteins, in combination with fluorescent ELIspot (FluoroSpot), ELISA, and intracellular cytokine staining, I have determined the frequency, cytokine secretion profile, effector function, and memory phenotype of CD4+ and CD8+ T cells in a large cohort of HCMV seropositive healthy donors. My results show that these viral gene products are also recognised by CD4+ T cells and are composed of distinct cellular populations secreting either IFN$\gamma$ or IL-10. The high sensitivity of this assay has also revealed previously uncharacterised CD8+ T cell responses to US28, UL111A, and UL144, as well as responses to LUNA and UL138. Intriguingly, IL-10 secretion by a distinct population of latency-specific CD8+ T cells was also observed. T cell responses to latency-associated ORF products were found to be composed of greater proportions of IL-10 secreting cells compared to responses to the lytic ORFs pp65, IE1, and gB. The frequencies of IL-10 secreting T cells specific to HCMV latency-associated proteins did not increase with greater time of viral carriage, as measured indirectly by donor age. Although IFN$\gamma$ secreting T cells specific to latency-associated proteins were detected in kidney transplant recipients immediately following primary HCMV infection, there were no such IL-10 secreting sub-populations, despite IL-10 T cell responses being detected to two lytic proteins, US3 and pp71. Given that latency-specific IL-10 secreting T cells were found to be a separate population to those secreting IFN$\gamma$, it was hypothesised that depleting the IL-10 secreting cells could improve the recognition and killing of latently infected cells by the specific but non-IL-10 producing T cell population. Classic regulatory T cells (Tregs) can be defined as CD4+CD127$^{lo}$CD25$^{hi}$, and depleting CD4+CD25$^{hi}$ cells was investigated as a means to remove the latent-specific IL-10 secreting T cells. The results showed that this had a variable effect, suggesting that HCMV-specific IL-10 secreting cells of this Treg phenotype represent only a proportion of the IL-10 secreting CD4+ T cell population. As this strategy could not provide a consistent method to remove IL-10 secreting CD4+ T cells, neutralising the effect of IL-10 and TGF$\beta$ using anti-cytokine and anti-receptor antibodies was tested. My initial data suggest that treatment of latently infected cells with these neutralising antibodies in the presence of CD4+ and CD8+ T cells reduced latent viral carriage.Medical Research Counci