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Laboratory findings in CD4(+) large granular lymphocytoses
H Olteanu1, N J Karandikar, C Eshoa
1Department of Pathology, Medical College of Wisconsin, Milwaukee, WI 53226, USA. holteanu@mcw.edu
Insights
CD4(+) T-cell large granular lymphocytic (LGL) leukemia is a distinct clonal disorder. This uncommon leukemia variant presents unique clinicopathologic features compared to the more frequent CD8(+) type.
Area of Science:
- Hematology
- Immunology
- Oncology
Background:
- Large granular lymphocytic (LGL) leukemia involves mature T or natural killer (NK) cells.
- Most T-LGL leukemia cases are CD3(+)/CD8(+), with rare CD4(+) variants reported.
Purpose of the Study:
- To describe the clinicopathologic features of aberrant CD4(+) cytotoxic T-cell lymphocytoses.
- To differentiate CD4(+) T-LGL lymphocytosis from the common CD8(+) variant.
Main Methods:
- Analysis of eight patients with CD4(+) cytotoxic T-cell lymphocytoses.
- Immunophenotyping for T-cell antigens (CD3, CD4, CD8, CD56, CD57).
- T-cell receptor gamma (Tgamma) gene rearrangement analysis (PCR).
Main Results:
- All patients had immunophenotypically aberrant CD4(+) T cells with uniform CD56 expression.
- Seven patients expressed CD57, and four showed partial dim CD8 expression.
- All cases were Tgamma PCR positive, indicating a clonal T-cell disorder.
Conclusions:
- CD4(+) T-LGL lymphocytosis is a clonal disorder.
- This variant exhibits distinct clinicopathologic characteristics compared to CD8(+) T-LGL leukemia.
- The condition appears to have a favorable prognosis without immediate need for therapy.
Abstract:
Large granular lymphocytic (LGL) leukemia is an uncommon disorder of mature T or natural killer (NK) cells. Most T-LGL proliferations are CD3(+)/CD8(+), although rare CD4(+) clonal T-LGL expansions have been reported. We report the clinicopathologic features of eight patients with aberrant CD4(+), cytotoxic T-cell lymphocytoses. Median follow-up was 29 months (range 8-100), during which all were alive without requirement for therapy. Four of eight patients had an additional malignancy; none had a history of rheumatoid arthritis, lymphadenopathy or hepatosplenomegaly. Morphologic expansions of granulated lymphocytes were evident in 6/8. All had immunophenotypically aberrant populations of CD4(+) T cells with uniform, moderate or bright CD56. Seven of eight expressed CD57, and four were CD8(partial dim +). Abnormal levels of expression of two or more T-cell antigens were seen in all cases. All tested cases were Tgamma PCR positive. Our results support that CD4(+) T-LGL lymphocytosis is a clonal disorder with clinicopathologic characteristics distinct from the more common CD8(+) variant.
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