November 10-15

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ACR Convergence 2023

San Diego, CA

Home // Carla M. Cuda, PhD: Neuropsychiatric symptoms of SLE

Carla M. Cuda, PhD: Neuropsychiatric symptoms of SLE


2 minutes

Poster presenter: Carla M. Cuda, PhD, Northwestern University

Poster title: Behavioral Deficits May Precede Influx of Brain-Infiltrating Macrophages in Neuropsychiatric Symptoms of Systemic Lupus Erythematosus

Poster Session B
8:30 – 10:30 a.m. ET Sunday, Nov. 7
All ACR Convergence 2021 poster presentations are available on demand to registered meeting participants through March 11, 2022.

What is your poster about?
Systemic lupus erythematosus (SLE) is a complex autoimmune disease that affects many end organs, including the brain. Despite a prevalence of over 50% among SLE patients, neuropsychiatric symptoms of SLE (NP-SLE), including anxiety and movement disorders, are among the least understood complications. Notwithstanding the paucity of data examining underlying mechanisms, accumulating evidence, including our own work, points to microglia, the resident innate immune cells in the brain, as a driver of disease. The crosstalk between infiltrating monocyte-derived macrophages and microglia plays a critical role in directing microglial responses. However, the question remains whether macrophage infiltration precedes NP-SLE manifestations. Here, we longitudinally investigated macrophage infiltration into the brain in two models of SLE.

Why did you decide to investigate this topic?
Our new data show that levels of macrophages in the brains of NP-SLE-prone mice are comparable to control levels at two months of age, yet behavioral deficits occur at two to three months of age in NP-SLE-prone mice. Here, we provide the first evidence that macrophage infiltration into the brain may be a response to NP-SLE-like disease incited by brain-intrinsic mechanisms rather than a cause. As diagnosis of NP-SLE is a challenge due to the lack of definitive causal mechanisms underlying the disease, our proposed use of multiple mouse models of NP-SLE allows us to interrogate these yet unknown causes of NP-SLE to inform diagnostic and therapeutic improvements.

What are you working on next related to this research?
Future studies will identify the exact timing of macrophage infiltration to define their role as either disease initiators or responders, and dissect macrophage heterogeneity during progression of NP-SLE-like disease.

What excites you most about your work?
Since diagnostic strategies for NP-SLE are limited, patients with NP-SLE often fail to achieve remission using current therapies, and side effects from treatment are substantial, the ultimate objective is to utilize these research discoveries to help in the development of targeted laboratory diagnostic tests as well as safer, more effective therapies for NP-SLE.