Reaserch progress of complement receptors involved in animal models of disease / 医学研究生学报

Complement receptor of the immunoglobulin superfamily ( CRIg) can regulate immune reactions via T cells and cy-tokines and is involved in various diseases .The effect of CRIg on the pathogenesis of immunological liver injury , intestinal ischemia-reperfusion injury , type Ⅰdiabetes mellitus , experimental autoimmune uveoretinitis , and rheumatoid arthritis etc .in animal models of disease are reviewed in this article .

Advance in The Neural Adhesion Molecule CHL1 in Nervous System / 生物化学与生物物理进展

Cell adhesion molecules(CAMs) play important roles in specifying cell-cell interactions during development,regeneration,and modification of synaptic activity.The close homolog of L1(CHL1) ,a recently identified member of the immunoglobulin superfamily of cell adhesion molecules,is localizably expressed in the nervous system.CHL1 interacts with like molecules(homophilic interaction) and non-like molecules(heterophilic interaction) on neighboring cells or the extracellular matrix to regulate axon outgrowth and fasciculation,neuronal migration and survival,synaptic plasticity and regeneration after trauma.

Functions of Siglecs in Allergic Inflammation / 소아알레르기및호흡기학회지

Siglecs are sialic acid binding Ig-like lectins, subset of the immunoglobulin superfamily. They are characterized by a homologous N-terminal V-set Ig-like domain and C2 set Ig-like domains. N-terminal domains have sialic acid binding activity. In humans, 11 Siglecs have been described sialoadhesin(Siglec-1), CD22(Siglec-2), CD33(Siglec-3), MAG(Siglec-4), more recently described CD33-related Siglecs(Siglec 5-11). Siglecs express most signal via immunoreceptor tyrosine-based inhibition motif(ITIM) cytoplasmic domains. The cytoplasmic tails of all Siglecs except sialoadhesin have one or more tyrosine residues within potential signaling motifs. Inhibitory function of other Siglecs such as Siglec-7 or Siglec-9 was shown in RBL-2H3 cells. Co-crosslinking of Siglec-7 or Siglec-9 and Fc epsilon R1 substantially reduced the serotonin release of RBL-7 and RBL-9 cells. Siglec-8 is expressed on human eosinophils, mast cells and basophils. Siglec-8 has two tyrosine motifs, a proximal motif and a distal motif. They have some inhibitory functions in immune system. We have observed that Siglec-8 is able to inhibit the IgE receptor-mediated beta-hexosaminidase release of RBL-2H3 cells following co-crosslinking. Co-crosslinking of Siglec-8 and Fc epsilon R1 reduced the hexosaminidase release of RBL-2H3 cells. These results show that Siglec-8 is as potent as Siglec-7 and Siglec-9 in delivering inhibitory signals to RBL-2H3 cells. Siglec-8 should be a new member of the inhibitory receptor superfamily and the membrane-proximal ITIM is essential for the inhibitory function of Siglec-8 molecules. Although these molecules present specific marker for the allergic cell types, more work is needed to understand the signaling mechanism and the role in various disease processes.

Role of adhesion molecules in neutrophil-mediated inflammation / 中国药理学通报

Adhesion molecules are involved in neutrophil-mediated inflammation. Neutropil adhesion to endothelial cell mediated by cell adhesion molecules (CAMs) is the first and critical step during the process of inflammation. Three families of CAMs play a central role in neutrophil-endothe-lial cell interactions : the selectins, the integrins, and the immunoglobulin superfamily. These different types of CAMs interact in a programmed, sequential manner to form neutrophil-endothelial cell adhesion cascade. The initial phase of inflammation, neulrophil slowing and rolling, is mediated by selectins; subsequently, firm adhesion of neu-trophils to vessel endothelial cells occurs via binding of the activated integrins and the endothelial receptors such as intercellular adhesion molecule-1 (ICAM-1); Then, neutrophils transmigrate into the tissues, this process requires chemotactic factors, integrins and PEC AM-1. Because of the important role of CAMs in the process of inflammation. Agents may be used to block the function of CAMs as a strategy of antiinflammatory therapy.