BaSed on information in this pdf make notes for md dermatology exam on emperipolesis
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emperipolesis Rosai-Dorfman
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emperipolesis histiocyte engulfing lymphocyte Rosai-Dorfman disease histology
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Emperipolesis - MD Dermatology Exam Notes
1. Definition
- Emperipolesis: "The active penetration of one cell by another which remains intact" (Humble, Jayne, Pulvertaft, 1956).
- Etymology (Greek): em = inside, peri = around, polemai = wander about.
- The engulfed ("passenger") cell stays viable and structurally intact inside the host cell and can exit at any time without harming either cell.
2. Emperipolesis vs Phagocytosis vs Entosis (key comparison - favorite exam point)
| Feature | Emperipolesis | Phagocytosis | Entosis |
|---|---|---|---|
| Fate of engulfed cell | Remains viable/intact, can exit | Destroyed by lysosomal enzymes | Homogenous cell-in-cell process (described by Overholtzer et al., 2007), similar appearance to emperipolesis but a distinct non-apoptotic cell death mechanism |
| Cell types | Histiocytes/megakaryocytes engulfing another living cell | Macrophage engulfing debris/microbes | Epithelial/tumour cells |
- Note: Entosis is often confused with emperipolesis on histology because it looks similar ("cell-in-cell") but the mechanism and outcome differ.
3. Cells Involved
- Host (engulfing) cells: mainly histiocytes and megakaryocytes.
- Passenger (engulfed) cells: lymphocytes, plasma cells, myeloid cells, erythroblasts, neutrophils. Also seen with tumour giant cells, Reed-Sternberg cells.
- Occurs in both physiological and pathological states.
4. Classification (high-yield)
- Megakaryocytic emperipolesis - engulfment of hematopoietic cells (erythroblasts, myeloid cells, neutrophils) by megakaryocytes.
- Seen in: Hodgkin's disease, leukaemias (acute/chronic myeloid), Non-Hodgkin's lymphoma, myeloproliferative disorders, myelodysplastic syndrome (MDS).
- Histiocytic emperipolesis - engulfment of inflammatory cells (lymphocytes, plasma cells) by histiocytes.
- Seen in: Rosai-Dorfman Disease (RDD) / Sinus Histiocytosis with Massive Lymphadenopathy (SHML) - the classic/hallmark association.
5. Diseases Associated with Emperipolesis
- Rosai-Dorfman disease (SHML) - hallmark/pathognomonic feature.
- Hematolymphoid disorders: Hodgkin's disease, leukaemias, Non-Hodgkin's lymphoma, myeloproliferative disorders, MDS.
- Non-hematological malignancies: multiple myeloma, neuroblastoma, rhabdomyosarcoma.
6. Histiocyte Morphology in SHML
- Round to oval, vesicular or hyperchromatic nuclei with distinct nucleoli.
- Abundant amphophilic to eosinophilic, granular or clear cytoplasm.
- Immunophenotype: shows features of BOTH antigen-presenting (Langerhans-like, S100 positive) and phagocytic histiocyte lines (alpha-1-antitrypsin, lysozyme, CD68, MAC-387 positive; CD1a negative).
7. Proposed Mechanism (Wang & Li hypothesis - important for viva)
- Emperipolesis may act as a pathway mediating NK-cell-mediated tumour cell killing.
- Requires target cell membrane fluidity for NK cell binding.
- Once inside the host/tumour cell, the NK cell can undergo mitosis.
- Tumour cell disintegration occurs via a lysosome-mediated degradation pathway at the ultrastructural level.
- Requires: extracellular free calcium, adhesion molecules, actin-based cytoskeleton.
- Disease-specific hypotheses:
- In SHML: recruitment of marrow monocytes from peripheral blood with early transformation into immunophenotypically distinct histiocytes.
- In myeloproliferative disease: increased P-selectin (adhesion molecule) expression → neutrophil sequestration on megakaryocyte surface → increased neutrophil-megakaryocyte interaction.
8. Fate of the Invading Cell (4 possible outcomes)
- Cannibalism - invading cell disintegrates via lysosome-mediated pathway.
- Host cell death via lysosome-mediated pathway.
- Transcytosis - invading cell passes through and exits.
- Syncytial - both invading and recipient cells undergo cell division.
9. Differential Diagnosis of SHML Histiocytes (exam tables - very testable)
SHML vs Langerhans Cell Histiocytosis (LCH)
| Feature | SHML | LCH |
|---|---|---|
| CD68 | ++ | -- |
| CD1a | -- | ++ |
| Birbeck granules | -- | ++ |
| Eosinophils as component | -- | ++ |
| Nuclear lobation | -- | ++ |
| Indentation/longitudinal grooving | -- | ++ |
SHML vs Malignant Melanoma (MM)
| Feature | SHML | MM |
|---|---|---|
| S100 | ++ | ++ |
| HMB-45 | -- | ++ |
| Emperipolesis | Present | Absent |
SHML vs Hodgkin's Disease (HD)
| Feature | SHML | HD |
|---|---|---|
| Matted lymph nodes | -- | ++ |
| Capsular fibrosis | -- | ++ |
| Reed-Sternberg cells | -- | ++ |
| CD15 | -- | ++ |
10. One-Line Summary for Rapid Revision
- Emperipolesis = live cell wandering inside another live cell, reversible, no destruction.
- Classic association = Rosai-Dorfman disease / SHML (histiocytic emperipolesis; S100+, CD68+, CD1a-).
- Also seen in megakaryocytes (megakaryocytic emperipolesis) in MDS/myeloproliferative disorders/leukemias.
- Distinguish from phagocytosis (engulfed cell destroyed) and entosis (distinct non-apoptotic cell-in-cell death, Overholtzer 2007).
- Mechanism still not fully elucidated; leading hypothesis involves NK-cell mediated, lysosome-dependent tumour cell killing requiring calcium, adhesion molecules, and actin cytoskeleton.
Source
- Rastogi V, Sharma R, Misra SR, Yadav L, Sharma V. "Emperipolesis - A Review." Journal of Clinical and Diagnostic Research. 2014 Dec;8(12):ZM01-ZM02. DOI: 10.7860/JCDR/2014/10361.5299 (the attached PDF).
Note on currency: This 2014 review remains the standard concise summary used in pathology teaching; the core mechanism, classification, and SHML differentials it describes are still current. Recent (2024-2026) systematic reviews have focused specifically on clinical presentation/treatment of Rosai-Dorfman disease at various sites, without contradicting the histopathologic/mechanistic content above - for further reading if your exam covers clinical management of RDD:
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