Publications by authors named "T P Dykstra"

Despite the presence of strategically positioned anatomical barriers designed to protect the central nervous system (CNS), it is not entirely isolated from the immune system. In fact, it remains physically connected to, and can be influenced by, the peripheral immune system. How the CNS retains such responsiveness while maintaining an immunologically unique status remains an outstanding question.

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Background: The COVID-19 pandemic has spread through pre-existing fault lines in societies, deepening structural barriers faced by precarious workers, low-income populations, and racialized communities in lower income sub-city units. Many studies have quantified the magnitude of inequalities in COVID-19 distribution within cities, but few have taken an international comparative approach to draw inferences on the ways urban epidemics are shaped by social determinants of health.

Methods: Guided by critical epidemiology, this study quantifies sub-city unit-level COVID-19 inequalities across eight of the largest metropolitan areas of Latin America and Canada.

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Traumatic injuries to the central nervous system (CNS) afflict millions of individuals worldwide, yet an effective treatment remains elusive. Following such injuries, the site is populated by a multitude of peripheral immune cells, including T cells, but a comprehensive understanding of the roles and antigen specificity of these endogenous T cells at the injury site has been lacking. This gap has impeded the development of immune-mediated cellular therapies for CNS injuries.

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The arachnoid barrier delineates the border between the central nervous system and dura mater. Although the arachnoid barrier creates a partition, communication between the central nervous system and the dura mater is crucial for waste clearance and immune surveillance. How the arachnoid barrier balances separation and communication is poorly understood.

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Aging is a complex process involving various systems and behavioral changes. Altered immune regulation, dysbiosis, oxidative stress, and sleep decline are common features of aging, but their interconnection is poorly understood. Using Drosophila, we discover that IM33, a novel immune modulator, and its mammalian homolog, secretory leukocyte protease inhibitor (SLPI), are upregulated in old flies and old mice, respectively.

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