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Immunosuppression versus tolerance is a primary criterion underlying the evaluation of immune therapy in type 1 diabetes.

Genetic mutations that cause vascular anomalies have been identified (e.g., TEK mutations cause mucocutaneous venous malformation). Animals carrying such genetic defects will be used to develop therapies.

Each year, 2.5 million people are infected with HIV. Although multiple prevention strategies exist, they must be effective, affordable, and population-specific.

The VEGF-family member PlGF appears to be dispensable for normal development and health. However, altering expression levels of PlGF can aggravate or counteract various disease conditions (e.g., tissue ischemia, malignancy, and inflammation).

Neurons rely on the proteasome and lysosomal systems to remove damaged proteins and organelles. Their disruption leads to the accumulation of toxic proteins—including amyloid-β and tau.

In pancreatic β cells, every type 1 diabetes autoantigen including (pro)insulin, GAD65, ZnT8, IA2, and ICA69 is connected to the secretory pathway.

All Parkinsonian disorders display nigrostriatal dopaminergic degeneration. But they are increasingly classified by underlying pathology (α-synucleinopathies, tauopathies, and TDP-43 proteinopathy).

The HIV envelope protein binds to the host cell receptor CD4 and then to a cellular coreceptor. This triggers fusion of the viral and host cell membranes, initiating infection.

Parkinson's disease involves apoptosis, autophagic cell death, and programmed necrosis. The contribution of each depends on the stimulus or stressor, its concentration and timing, and brain region or cell type.

Alzheimer disease is the most frequent cause of dementia in Western societies. Advancing age and genetic and nongenetic antecedent factors (e.g., education and obesity) are thought to play important roles.