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Biomedical subjects

R Marcotte

Publications and source records attributed to R Marcotte.

5 recordsLinked to original sources

Signaling pathway for apoptosis: a racetrack for life or death.

Apoptosis, or programmed cell death, is a gene-directed mechanism activated as a suicidal event to get rid of excess, damaged, or infected cells. The recent astounding pace of research in this area has expanded our horizon of understanding that this mechanism is regulated largely by pro- and anti-apoptosis factors acting for or against the final death event. The driving force behind these factors, either pro-apoptosis or pro-survival, is largely determined by signal transduction pathways, starting with the initiation of a death signal at the plasma membrane, and following through a complex cytoplasmic network before reaching the end point of cell demise. Enmeshed in this intricate cytoplasmic network are many checkpoints, where complexes of pro- and anti-apoptosis factors function to facilitate or deter the death signals. The culmination of the balancing act between these two camps of factors at these signal transduction checkpoints may then result in the final decision to die or to live. Thus, the eventual death of a cell may require successful passage through all the checkpoints, a mechanism Nature has provided as a safeguard to prevent erroneous triggering of death. With the advent of a new biotechnology revolution at the dawn of the new millenium, we look forward to an exciting era when we can gain fuller understanding of the operation of all these checkpoints. Ultimately, this gain will pave the way to control the apoptosis event at the checkpoints, and to support the organism's functionality as long as possible. J. Cell. Biochem. Suppls. 32/33:95-102, 1999.

Animals↗

Cytokine-induced differentiation of precursor mouse CD8+ T cells into cytotoxic CD8+ T cells secreting Th1 or Th2 cytokines.

Alloantigen-stimulated CD8+ mouse spleen cells, either spontaneously or in the presence of IL-12 or IFN gamma plus anti-IL-4, differentiate into CD8+ T cells secreting a Th1-like cytokine pattern (IL-2 and IFN gamma). IL-4 induced differentiation into CD8+ T cells secreting Th2 cytokines (IL-4, IL-5, IL-6, and IL-10), whereas anti-IFN gamma suppressed the development of CD8+ cells secreting IFN gamma. Clones of IL-4- or IFN gamma-producing CD8+ T cells were relatively stable, as IL-4 or IFN gamma did not cause interconversion of committed CD8+ T cells. Both CD8+ subsets were cytotoxic, failed to provide cognate help for B cell antibody production, and remained CD4-, CD8 alpha+ CD8 beta+. We propose the names TC1 and TC2 for cytotoxic CD8+ T cells secreting Th1-like and Th2-like cytokines, respectively.

Animals↗

Quo vadis?

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Career Choice↗