CD16 (FcγRIII) is commonly used as a marker for NK cells, especially the cytotoxic CD56dim subset, and mediates antibody-dependent cellular cytotoxicity. However, it is not exclusive to NK cells — monocytes, macrophages and neutrophils also express CD16 — and some NK cells (CD56bright) lack CD16. Thus it identifies NK subsets but is not NK-specific.

High NK CD56+CD16+ indicates an increased number of natural killer cells with CD56 and CD16 markers, reflecting raised cytotoxic NK activity. Causes include recent or ongoing viral infection, inflammation, stress, autoimmune conditions, or less commonly an NK‑cell proliferative disorder. Clinical significance depends on symptoms and degree of elevation; follow up with your clinician for correlation and possible repeat testing or hematology referral.

Most NKT cells do not constitutively express CD16 (FcγRIII). Classical/invariant NKT cells typically lack strong CD16 expression, although some human NKT-like or activated CD56+ NKT subsets can express CD16 and perform antibody-dependent cellular cytotoxicity. Thus CD16 is variable and not a defining marker for NKT cells; expression depends on subset, activation state, and species.

CD56 is the neural cell adhesion molecule (NCAM) commonly used as a marker of natural killer (NK) cells (CD56bright and CD56dim subsets) and some cytotoxic T‑cell (NKT) subsets. It is also expressed on neural and neuroendocrine tissues and is used diagnostically to identify neural‑ or neuroendocrine‑derived tumors such as neuroblastoma and small‑cell lung carcinoma.

CD56bright CD16− NK cells are less cytotoxic, produce cytokines (e.g., IFN-γ), and are enriched in lymphoid tissues. CD56dim CD16+ NK cells are more mature, predominate in peripheral blood (~90%), express CD16 (FcγRIIIa) for antibody-dependent cellular cytotoxicity, and have higher direct killing activity. The markers indicate a division between cytokine-driven regulation and cytotoxic effector function.

No — parental NK-92 cells do not express CD16 (FcγRIII); they are typically CD56bright and CD3−, CD16−. Because this limits natural antibody-dependent cellular cytotoxicity (ADCC), many research and clinical programs use genetically modified NK-92 variants that are engineered to express CD16 (often the high-affinity 158V form) to enable or enhance ADCC.