T-cell receptor biases and clonal proliferations in blood and pleural effusions of patients with lung cancer.
Hum Immunol
; 53(1): 39-48, 1997 Mar.
Article
em En
| MEDLINE
| ID: mdl-9127146
ABSTRACT
We sought evidence that pulmonary carcinomas mediate a cellular immunologic response by analyzing T-cell antigen receptor beta-chain variable gene (TCRBV) repertoires of lymphocytes from peripheral blood (PBL) and malignant pleural effusions (PEL) of five lung cancer patients. Expression levels of 27 TCRBV were quantitated by multiprobe RNase protection assay (RPA), and clonal expansions were identified by sequence enrichment nuclease assay (SENA) and junctional region sequencing. Abnormal TCRBV expansions were identified in all subjects by RPA (mean 6.9 +/- 1.7/patient), and their number closely correlated with elapsed time since initial diagnosis (r = 0.97). SENA, performed in specimens from three patients, confirmed the presence of mono or oligoclonality in 48% of abnormal RPA expansions, and further identified T-cell clones among TCRBV with normal expression levels. The majority of clonal expansions were among PEL, and were nearly equally divided between CD4 and CD8. These data show that T-cell repertoires of lung cancer patients are characterized by marked abnormalities and frequent clonal expansions, most likely representing responses to unique, tumor-specific antigens (TSA). Moreover, this process appears exaggerated among PEL, further suggesting that malignant effusions include local proliferations of tumor reactive T cells. These findings imply the presence of lung cancer TSA capable of eliciting cellular immune responses and raise the possibility that selective immunotherapies can ultimately be developed.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Carcinoma Broncogênico
/
Linfócitos T
/
Derrame Pleural Maligno
/
Receptores de Antígenos de Linfócitos T alfa-beta
/
Neoplasias Pulmonares
Tipo de estudo:
Prognostic_studies
Limite:
Aged
/
Humans
Idioma:
En
Ano de publicação:
1997
Tipo de documento:
Article