Calreticulin, a calcium-binding, multifunctional protein, involved in calcium storage has been suggested a target in the disease initiation, and antibodies to calreticulin have been demonstrated in sera from mothers with affected children [46]. Another suggested antibody specificity associated with congenital heart block is antibodies to p57, which was identified in a child with the disease [47]. Antibodies to a cleavage product

of α-fodrin has, in addition to being identified as an organ-specific antibody in Sjögren’s syndrome, been suggested as an additional serologic marker in congenital GSI-IX solubility dmso heart block [48]. Lately, Llanos and colleagues [49] investigated the role of antibodies to α-enolase associated with the condition, but a relationship could not be confirmed. Congenital heart block is considered a passively acquired disease where maternal antibodies against Ro/La antigens are potentially affecting the developing foetal heart resulting in a complete atrioventricular block. No antibody specificity has been closer associated with congenital heart block than anti-Ro52 antibodies, which are detectable in the vast majority of autoantibody-positive

mothers of affected children. this website However, considering clinical observations of only 10–20% reoccurrence rate in Ro/La-positive mothers with a previously affected infant, this indicates that maternal autoantibodies are necessary but not sufficient for induction of disease. old Clinical factors such as maternal disease and infection [50–52] as well as antibody levels [13, 19, 51] and subclasses [19, 53] have been studied without reaching a common conclusion. A two-stage model for the development of congenital heart block has been suggested, including transferred anti-Ro52 antibodies as initiators of cell death and the cardiac insult. This reaction may in later phases be exaggerated by other autoantibodies targeting intracellular autoantigens now exposed on the cell surface resulting in permanent damage in genetically susceptible foetuses [54]. Remaining

questions are whether the binding of maternal autoantibodies is direct or indirect, as well as an explanation to why the foetal heart is selectively vulnerable compared to the adult maternal heart, and why congenital heart block only affects a small portion of foetuses in Ro52 seropositive women. Financial support for this work was obtained from KIRCNET (Karolinska Institutet Circulation and Respiratory Research Network), the Magn Bergvalls Foundation, the Jerring Foundation, Stiftelsen Samariten, the Karolinska Institute and The Royal Swedish Academy of Sciences. “
“Cyclin B1 is a checkpoint protein that regulates cell division from G2 to the M phase. Studies in mice have shown that cyclin B1 vaccine-induced immunity significantly delayed or prevented the spontaneous cancer development later in life.