Granulocyte colony-stimulating factor (G-CSF) and its PEGylated long-acting formulation (pegfilgrastim) are widely used to prevent chemotherapy-induced neutropenia and to mobilize peripheral blood stem cells in donors. Beyond granulopoiesis, G-CSF exerts context-dependent immunomodulatory effects that span innate and adaptive compartments, which helps explain why, in susceptible settings, exogenous stimulation may tip immune homeostasis toward inflammation [[1], [2], [3]]. In parallel, accumulating clinical observations have linked therapeutic G-CSF—particularly pegfilgrastim—to large-vessel vasculitis/aortitis and other neutrophil-dominant inflammatory phenotypes, including Sweet’s syndrome, neutrophilic dermatosis of the dorsal hands, crystal arthropathies, and rarer pulmonary complications [[4], [5], [6], [7], [8], [9], [10], [11], [12]]. Cohort-level signals indicate that the burden of pegfilgrastim-associated aortitis is low but non-negligible, with preferential involvement of the aortic arch and proximal branches and a typical latency of one to two weeks after dosing [4,5]. Against this background, mechanistic data highlighting G-CSF as a driver of autoinflammation in defined genetic contexts further strengthen the biological plausibility of these clinical signals [3].

In clinical practice, G-CSF is administered in two main ways: short-acting daily filgrastim and single-dose pegfilgrastim, which achieves higher and more sustained systemic exposure. These pharmacokinetic differences plausibly shape the timing and tissue tropism of adverse immune events—vascular inflammation clustering about one to two weeks after pegfilgrastim, and earlier cutaneous or articular presentations within days of exposure. Across cohorts and case series, a recognizable pattern emerges: new mural thickening/enhancement of the aortic arch and proximal branches on CT in often minimally symptomatic patients; negative autoimmune serologies; brisk improvement with drug withdrawal and, when needed, short glucocorticoid courses; and occasional recurrence on re-exposure that supports a drug-induced mechanism [[4], [5], [6], [7], [8], [9], [10], [11], [12]]. These observations, together with G-CSF’s broad effects on neutrophil priming and cytokine circuits, motivate a focused synthesis of G-CSF–associated immune toxicity that can inform bedside recognition and management [[1], [2], [3]].

The objective of this study was to identify and summarize reports in which exogenous G-CSF (filgrastim or pegfilgrastim) triggered or exacerbated autoimmune/rheumatic disease, and to describe clinical phenotypes, latency, management, and outcomes.