Hepatosplenic γδ T‐cell lymphoma following seven malaria infections

Pathology International - Tập 56 Số 11 - Trang 668-673 - 2006
Rocı́o Hassan1, Sergio A L Franco, Cláudio Gustavo Stefanoff, Sérgio Romano, Hilda Rachel Diamond, Luiz G P Franco, Héctor N. Seuánez, Ilana Zalcberg
1Bone Marrow Transplantation Center, National Institute of Cancer, Rio de Janeiro, RJ, Brazil. [email protected]

Tóm tắt

Hepatosplenic γδ T‐cell lymphoma (HSTL) is a clinicopathological entity associated with an immunocompromised status in approximately 25% of patients. Herein is described a case of HSTL in a 53‐year‐old Brazilian man with seven previous malaria infections, initially misdiagnosed as a hyperreactive splenomegaly due to chronic malaria. A characteristic lymphoid infiltrate was observed in spleen, liver and bone marrow sinusoids/sinuses. Neoplastic cells had a CD45RO+, CD2+, CD7+, CD3+, CD5–, CD8+, CD56+, perforin+, FasL‐negative, T‐cell receptor (TCR)αβ‐negative, TCRγδ+ profile. Analyses of γ and δ TCR rearrangements confirmed diagnosis of γδ T‐cell lymphoma by detecting VγI/Vδ1‐Jδ1 clonal rearrangements. Sensitive polymerase chain reaction (PCR) for Plasmodium falciparum, Epstein–Barr virus and herpesvirus‐8 failed to demonstrate infection. The disease progressed to a fatal outcome following cutaneous infiltration and leukemic proliferation. The authors also comment on the association of lymphoma and infection, focusing on PCR diagnosis of TCRγ and δ clonal rearrangements and the presumed pathogenic events leading to HSTL in the context of chronic malaria infection. Initial lymphomagenic stages might not be direct consequences of antigenic stimulation of Vδ1 T‐cells, but might depend on interactions between γδ T and B cells during cooperative or regulatory responses to Plasmodium sp.

Từ khóa


Tài liệu tham khảo

Persing DH, 1999, Infection, immunity and cancer, Arch Pathol Lab Med, 123, 1015, 10.5858/1999-123-1015-IIAC

10.1016/S0959-8049(01)00102-2

10.1007/s11926-003-0011-y

10.1016/0923-2494(91)90154-B

10.1002/ijc.2910060102

10.1038/nrmicro1089

10.1016/S0065-230X(08)60470-4

10.1016/0140-6736(92)92108-R

10.1038/sj.leu.2400878

10.1038/sj.leu.2401784

10.1046/j.1365-2559.2000.00893.x

10.1309/TC9U-FAV7-0QBW-6DFC

10.1182/blood-2003-05-1675

10.1016/S0140-6736(02)09680-0

10.1016/S0046-8177(97)90176-3

10.1097/00019606-200306000-00003

10.1038/sj.leu.2400825

10.1038/sj.leu.2400887

10.1007/s004360050173

10.1182/blood.V84.5.1361.1361

10.1016/0009-8981(91)90247-A

10.1016/0140-6736(91)91293-4

10.1038/nri797

10.1073/pnas.91.1.345

10.1645/0022-3395(2002)088[0059:PFAPVG]2.0.CO;2

Hayday AC, 2000, γδ cells: A right time and a right place for a conserved third way of protection, Ann Rev Immunol, 24, 3044

10.1016/S1471-4906(01)02110-X

10.1093/intimm/12.6.797

10.1128/IAI.69.5.3190-3196.2001

10.4049/jimmunol.171.10.4979

Li B, 1998, Involvement of the Fas/Fas‐ligand pathway in activation‐induced cell death of mycobacteria reactive human γδ T cells: A mechanism for the loss of γδ T cells in patients with pulmonary tuberculosis, J Immunol, 161, 1558, 10.4049/jimmunol.161.3.1558