This article details the development and validation of a measure of critical consciousness, defined as the capacity of oppressed or marginalized people to critically analyze their social and political conditions, endorsement of societal equality, and action to change perceived inequities. In Study 1, an exploratory factor analysis (EFA) was conducted with a diverse sample of youth, resulting in three internally consistent factors: (a) Critical Reflection: Perceived Inequality, (b) Critical Reflection: Egalitarianism, and (c) Critical Action: Sociopolitical Participation. In Study 2, a confirmatory factor analysis (CFA) was completed with a new sample of youth. Strong model fit estimates in Study 2 confirmed the factor structure of Study 1 and resulted in a final 22-item measure called the "Critical Consciousness Scale" (CCS). The CCS has the potential to unite and advance the fragmented conceptualization and measurement of critical consciousness, the primary motivation for the development of the scale.
Summary
The contribution of thymic antigen presenting cell (APC) subsets in selecting a selftolerant T cell population remains unclear. We show that bone marrow (BM) APCs and medullary thymic epithelial cells (mTECs) played non-overlapping roles in shaping the T cell receptor (TCR) repertoire by deletion and regulatory T (Treg) cell selection of distinct TCRs. Aire, which induces tissue-specific-antigen expression in mTECs, affected the TCR repertoire in a manner distinct from mTEC presentation. Approximately half of Aire-dependent deletion or Treg cell selection utilized a pathway dependent on antigen presentation by BM APCs. Batf3-dependent CD8α+ dendritic cells (DCs) were the crucial BM APC for Treg cell selection via this pathway, showing enhanced ability to present antigens from stromal cells. These results demonstrate the division of function between thymic APCs in shaping the self-tolerant TCR repertoire, and reveal an unappreciated cooperation between mTECs and CD8α+ DCs for presentation of Aire-induced self-antigens to developing thymocytes.
We turnover billions of apoptotic cells daily, and these are removed by professional and non-professional phagocytes via efferocytosis
1
. Characterizing the transcriptional program of phagocytes, we discovered a novel solute carrier family (SLC) gene signature (involving 33 SLC members) that is specifically modified during efferocytosis, but not antibody-mediated phagocytosis. Assessing the functional relevance of these SLCs, we noted a robust induction of an aerobic glycolysis program in efferocytic phagocytes, initiated by SLC2A1-mediated glucose uptake, with concurrent suppression of oxidative phosphorylation program. Interestingly, the different steps of phagocytosis
2
, i.e.
smell
(‘find-me’ signals/ sensing factors released by apoptotic cells),
taste
(phagocyte-apoptotic cell contact), and
ingestion
(corpse internalization), activated different SLCs and other molecules to promote glycolysis. Further, lactate, a natural by-product of aerobic glycolysis
3
, was released via another SLC (SLC16A1) that was upregulated after corpse uptake. While glycolysis within phagocytes contributed to actin polymerization and the continued uptake of corpses, the lactate released via SLC16A1 influenced the establishment of an anti-inflammatory tissue environment. Collectively, these data reveal a novel SLC program activated during efferocytosis, identify a previously unknown reliance on aerobic glycolysis during apoptotic cell uptake, and that glycolytic byproducts of efferocytosis can also influence other cells in the microenvironment.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.