Reed-Sternberg Cells : CD20
Image Description
Loss of B-cell Phenotype in Hodgkin and Reed-Sternberg (HRS) cells: HRS cells are derived from germinal center or post-germinal center B-cells. They show clonal and somatically mutated Ig heavy- and light-chain gene rearrangements in > 95% of cases of classic Hodgkin lymphoma (cHL).
However, there is no immunoglobulin expression and there is near total loss of classic B lineage markers such as CD19, CD20, CD22, and CD79a. Patchy, weak and heterogenous staining for CD20 is seen HRS cells in about 20% of cHL. Some HRS cells are negative. This image shows several CD20-negative HRS cells near the center.
The mechanisms underlying loss of B cell phenotype is thought to be a combination of promoter hypermethylation and epigenetic silencing of key regulators of B- and T-cell differentiation.
Under normal physiologic conditions, any germinal center B cells with non-functional immunoglobulin genes and lacking expression of surface B-cell receptors would be programmed to undergo apoptosis. However, HRS cells are rescued from apoptosis by constitutive activation of NF-κB pathway.
However, there is no immunoglobulin expression and there is near total loss of classic B lineage markers such as CD19, CD20, CD22, and CD79a. Patchy, weak and heterogenous staining for CD20 is seen HRS cells in about 20% of cHL. Some HRS cells are negative. This image shows several CD20-negative HRS cells near the center.
The mechanisms underlying loss of B cell phenotype is thought to be a combination of promoter hypermethylation and epigenetic silencing of key regulators of B- and T-cell differentiation.
Under normal physiologic conditions, any germinal center B cells with non-functional immunoglobulin genes and lacking expression of surface B-cell receptors would be programmed to undergo apoptosis. However, HRS cells are rescued from apoptosis by constitutive activation of NF-κB pathway.