@Article{ecn.2006.0032,
AUTHOR = {Yvonne Kalmbach, Angelica B. W. Boldt, Rolf Fendel, Benjamin Mordmüller, Peter G. Kremsner, Jürgen F. J. Kun},
TITLE = {Increase in annexin V-positive B cells expressing LILRB1/ILT2/CD85j in malaria},
JOURNAL = {European Cytokine Network},
VOLUME = {17},
YEAR = {2006},
NUMBER = {3},
PAGES = {175--180},
URL = {http://www.techscience.com/ECN/v17n3/66147},
ISSN = {1952-4005},
ABSTRACT = {The outcome of a <i>Plasmodium falciparum</i> infection differs greatly between patients, ranging from
an asymptomatic carrier status to the most severe characteristics influenced by activating and inhibiting immune
factors. The inhibitory leukocyte immunoglobulin-like receptor (LILRB1/CD85j) plays an important role in the
immune response as regulator of cytotoxic T cells and of premature activation and clonal expansion of B cells. To
investigate its role in malaria, we analyzed blood samples from malaria patients by cytometric analysis. We found
a similar expression pattern of CD85j on PBMC in both patients and healthy children. However, malaria patients
presented significantly more CD85j
<sup>+</sup>
CD19<sup>+</sup> B cells, which also bound annexin V an indicator of early cell death.
We compared the plasma levels of several cytokines, since it was speculated that CD85j expression influences
cytokine release. Production of inflammatory cytokines was significantly increased in severe malaria cases. We
suggest that in malaria, dying B cells contribute to the overwhelming cytokine release and the impairment of the
immune memory.},
DOI = {10.1684/ecn.2006.0032}
}