Super-ego: ego tenant

The process of metapsychologic concepts development in Freud`s works is not linear; on the contrary, it oscillates, with comings and goings, temporary abandonments, ambiguities, contradictions. Within key metapsychology concepts, the concept of superego is certainly complex and troublesome, for not only it holds many definitions but its scope is also wide. From clinic to metapsychology, going across the theory of culture, the superego plays a role in all aspects of psychoanalytic investigation, misunderstandings appearing quite frequently, therefore, among those who comment it. In addition to it, Freud himself was no faithful historian of his own concepts. The present paper proposes to undo a few ambiguities in what concerns the evolution process of ego conception, beginning from a fundamental metapsychologic problem, which is the remake of the notion of ego. We support that changes in the ego theory were crucial to the elaboration of conceptual basis of super-ego in its legislative function. We will see that the super-ego begins its story as a discreet tenant to the ego to become tyrannical and usurper, threatening the ego integrity.

Autoimmune regulator (AIRE) contributes to Dectin-1-induced TNF-alpha production and complexes with caspase recruitment domain-containing protein 9 (CARD9), spleen tyrosine kinase (Syk), and Dectin-1

Background: Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) syndrome is a complex immunologic disease caused by mutation of the autoimmune regulator (AIRE) gene. Autoimmunity in patients with APECED syndrome has been shown to result from deficiency of AIRE function in transcriptional regulation of thymic peripheral tissue antigens, which leads to defective T-cell negative selection. Candidal susceptibility in patients with APECED syndrome is thought to result from aberrant adaptive immunity. Objective: To determine whether AIRE could function in anticandidal innate immune signaling, we investigated an extrathymic role for AIRE in the immune recognition of beta-glucan through the Dectin-1 pathway, which is required for defense against Candida species. Methods: Innate immune signaling through the Dectin-1 pathway was assessed in both PBMCs from patients with APECED syndrome and a monocytic cell line. Subcellular localization of AIRE was assessed by using confocal microscopy. Results: PBMCs from patients with APECED syndrome had reduced TNF-alpha responses after Dectin-1 ligation but in part used a Raf-1-mediated pathway to preserve function. In the THP-1 human monocytic cell line, reducing AIRE expression resulted in significantly decreased TNF-a release after Dectin-1 ligation. AIRE formed a transient complex with the known Dectin-1 pathway components phosphorylated spleen tyrosine kinase and caspase recruitment domain-containing protein 9 after receptor ligation and localized with Dectin-1 at the cell membrane. Conclusion: AIRE can participate in the Dectin-1 signaling pathway, indicating a novel extrathymic role for AIRE and a defect that likely contributes to fungal susceptibility in patients with APECED syndrome. (J Allergy Clin Immunol 2012;129:464-72.)