CR1 (Complement C3b/C4b Receptor 1)

Interactions between B cells and the complement system via CR1 (CD35) and CR2 (CD21), together with dysfunction of the blood-brain barrier (BBB) and blood-nerve barrier (BNB), may facilitate parallel immune activation across both compartments. In this case, the observed radiological and electrophysiological stabilization under anti-CD20 therapy is consistent with a B-cell-driven pathogenic model in CCPD.

The mass showed significantly increased FDG uptake. The patient underwent surgical resection, and histopathologic examination revealed a spindle cell tumor positive for CD21 and CD35, confirming the diagnosis of FDCS.

FDCS has a unique histological morphology and immunophenotype for FDCS. It is rare for FDCS to occur in the lungs. However, owing to the lack of experience among doctors and the limitations of small biopsy specimens, FDCS can easily be misdiagnosed as lung cancer. When tumour cells exhibit the above histological features, additional immunostaining for FDC markers should be performed. The Clinical Trial Number is ChiCTR2400090730 and Reg Date is October 12, 2024.

FDCS is a rare neoplasm with variable morphologic and staining patterns. To the best of our knowledge, this is the first reported instance of pleura-based FDCS with epithelioid morphology and aberrant expression of cytokeratins. Diagnosis of such cases can be challenging, which has to be separated from the morphologic mimicries, particularly carcinoma and mesothelioma.

Initial therapy comprised high-dose methylprednisolone, intravenous immunoglobulin and thalidomide, followed by surgical resection and adjuvant thalidomide-cyclophosphamide-prednisone. Postoperatively, inflammatory indices normalized and mucocutaneous lesions partially improved; nevertheless, the patient died of respiratory failure 6 months after surgery. In summary, the present case report aimed to provide valuable references and experiences for clinicians in the diagnosis and treatment of CD featuring PNP and FDCS.

Occasionally, it can overlap with follicular dendritic cell sarcoma by morphology and immunophenotype, which can lead to misdiagnosis. Only by combining clinical information, morphological characteristics and immunophenotype can an appropriate diagnosis be made.

Most cases follow an indolent clinical course and have a favorable prognosis after complete surgical resection, though rare aggressive cases have been reported. Understanding its clinicopathological and molecular features is essential for accurate diagnosis and management.

In neoplastic tissue, slower cellular dynamics and fewer interactions were observed compared to reactive tissue. This indicates differences in cellular behavior between reactive and neoplastic tissues, with a more dynamic cellular environment observed in reactive tissue.

Genetic or epigenetic-mediated CR1 deficiency is a potential hallmark of CAPS and predicts response to C5 inhibition.

Gastric FDCS is easily misdiagnosed as gastrointestinal stromal tumor (GIST) or Castleman disease due to overlapping imaging features. Multimodal imaging (CT, MRI, positron emission tomography/CT) combined with histopathology is critical for accurate diagnosis. Radical surgery remains the cornerstone of treatment, emphasizing the need for wide resection to minimize recurrence. This case provides the first comprehensive imaging characterization of gastric FDCS, enhancing awareness and diagnostic precision for this rare entity.

The subsequent analysis revealed a complex protein regulation network that influenced lipid traits. Furthermore, we used cis-MRBEE to discover that the expressions of CR1 in the basal ganglia, hippocampus, and oligodendrocytes were potentially causal for Alzheimer's disease and its biomarkers, A$beta $42 and pTau, in cerebrospinal fluid.