Characterization of a neoplastic B cell clone that secretes IgM in response to Th2-derived lymphokines.

Autor: Brooks KH; Department of Microbiology, Michigan State University, East Lansing 48824-1101., Oakley CS, Takayasu H
Jazyk: angličtina
Zdroj: The Journal of molecular and cellular immunology : JMCI [J Mol Cell Immunol] 1990; Vol. 4 (6), pp. 339-47; discussion 347-8.
Abstrakt: Recent advances of T cell cloning have allowed the classification of T helper cells in terms of the lymphokines they secrete. The functional significance of segregating lymphokine production to unique T cell subsets is still being evaluated, but undoubtedly plays a key role in the regulatory mechanisms of the immune system. Initial studies have indicated that the Th1 cells which secrete IL-2 and IFN-gamma may be primarily responsible for augmenting cell-mediated responses, whereas Th2 cells, which release IL-4, IL-5, and IL-6, provide help for humoral responses. However, it is also known that B cells can respond to both IL-2 and IFN-gamma. This raises the question of the homogeneity of B lymphocyte activation requirements. Are all B cells responsive to all of the lymphokines with the end-result of stimulation depending largely on the relative concentrations of the various lymphokines, or are there B cell subsets which only respond to Th1-derived lymphokines and others which respond to Th2-derived lymphokines? Such differential activation requirements might be present to allow these subsets to play unique roles in immunological responses. Since B cell cloning techniques have not yet been developed to obtain a homogenous B cell population for studies of activation requirements, regulation of lymphokine receptors, and regulation of gene expression, we must utilize lymphokine-responsive neoplastic B cells. The vast majority of spontaneous B cell lymphomas appear to belong to a minor B cell subset which expresses the Ly1 marker. This subset is clearly not representative of the majority of splenic B cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Databáze: MEDLINE