
Impairment of T‐cell functions with the progressive ascitic growth of a transplantable T‐cell lymphoma of spontaneous origin
Author(s) -
Shanker Anil,
Singh Sukh Mahendra
Publication year - 2000
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2000.tb01437.x
Subject(s) - biology , cd8 , immune system , t cell , interleukin 2 , t lymphocyte , lymphoma , involution (esoterism) , cytolysis , immunology , cytotoxic t cell , medicine , in vitro , endocrinology , consciousness , biochemistry , neuroscience
It has been observed that the progressive ascitic growth of a transplantable T‐cell lymphoma of spontaneous origin, designated Dalton's lymphoma (DL), in a murine host induces inhibition of various immune responses and is associated with an involution of thymus accompanied by a massive depletion of the cortical region and alteration in the distribution of thymocytes caused by tumour serum‐dependent induction of apoptosis with a decrease of CD4 + CD8 + , CD4 + CD8 − and CD4 − CD8 + thymocytes. Here, we report that thymocytes of DL‐bearing mice are defective in their proliferative ability and in their response to non‐specific mitogenic stimulus in vitro. Also, antigen‐specific T‐cell proliferative ability representing the fundamental T H function declines under DL‐bearing conditions and upon treatment with serum of DL‐bearing mice. Moreover, a significant inhibition of T‐cell cytolytic activity with a decreased ability to produce interferon γ is shown by the T cells of DL‐bearing mice and by the T cells treated with DL‐ascitic fluid, DL‐conditioned medium or serum of DL‐bearing mice. Further, addition of interleukin‐2 and anti‐interleukin‐10 to the cultures of thymocytes treated with serum of DL‐bearing mice is found to inhibit the induction of apoptosis in thymocytes, a phenomenon associated with the progression of DL growth. Analysis of the results indicates an immune deviation with the predominance of a T H2 ‐type response with the progression of tumour. We further discuss the possible mechanisms that may explain the observed tumour‐induced diminution of T‐cell immunity.