Lymphocyte-mediated Immune Responses Research Articles

Giant cell myocarditis

The present report describes a 45-year-old man with giant cell myocarditis who died of heart failure eight months after the onset of symptoms. On postmortem examination, the heart showed extensive myocardial fibrosis with numerous multinucleated giant cells. The lungs and a series of 20 lymph nodes showed no evidence of granulomatous disease, thereby excluding a diagnosis of sarcoldosis. Circumstantial evidence supports the view that giant cell myocarditis may have an autoimmune origin, and the histopathology suggests that cellular immune mechanisms might have a role in the pathogenesis of this disease. On this basis, it is suggested that cyclosporine, a selective inhibitor of T lymphocyte-mediated immune responses, may be useful for the treatment of this presently fatal disease.

Cyclosporin A-treated guinea pig responder cells secrete a genetically restricted factor that suppresses the mixed leukocyte reaction.

Cyclosporin A (CY A) is a hydrophobic, undecapeptide, fungal metabolite with potent immunosuppressive effects on T lymphocyte-mediated immune responses. Suppressor T lymphocytes generated during a mixed leukocyte reaction (MLR) performed in the presence of CY A, release a factor that suppresses a primary MLR of responder T cells, which is derived from the same strain as the factor producer but lacks specificity for the stimulator cell. These results suggest a finely regulated pathway by which CY A may induce and maintain a permanent state of transplantation tolerance in vivo.

Lymphocyte-mediated immune responses in neoplasia.

All or most immune responses to neoplasms may be considered to be mediated by subpopulations of lymphoid cells. Those immune responses to tumors which are directed specifically against tumor-associated antigens and which effect primarily “cellular” immune responses are discussed. “Humoral” immune responses to tumor-associated antigens are considered only insofar as they interact with “cellular” responses. In addition, the mediation of cellular immune responses to tumor antigens by lymphoid extracts, i.e., “immune” RNA and transfer factor, is described. Although research utilizing animal models is discussed where appropriate or necessary, this report stresses studies of lymphocyte-mediated immune responses to human tumors.