The late clinical manifestations that arise when bioimplants are applied seem to have an immunologic basis. We are studying both the histological characteristics and the lesional mechanisms of the most frequently used implants. We try to analyze the role that bacteria may have in the induction and/or maintenance of these reactions and the possible correlation between particular HLA haplotypes and the adverse effects.

Around 2-3% of reproductive-age couples suffer recurrent pregnancy loses. Almost 18% of couples that wish to have children suffer infertility problems. Simultaneously, 2-3% of all pregnant women are diagnosed with spontaneous loses. The expression of HLA molecules, specially type G, the degree of trophoblastic apoptosis, the outsourcing of new neoantigens such as phospholipids, the balance between Th1/Th2/Th3 cytokines, the type and quantity of CD4+CD25+Foxp3+ lymphocytes, the kind and the activity of uterine NK cells (uNK) cells, the presence or absence of blocking antibodies, and other mechanisms play different roles in the achievement of the so-called "tolerant microenvironment" needed to develop a normal pregnancy. Therefore, both autoimmune and alloimmune mechanisms are important. We aim at studying which isolated, and specially associated, anomalies can be identified as risk markers to be able to evaluate possible treatments.

This research line is centered into the study of the role of cross-reactivity among oxidized lipoproteins (oxLDL), antiB2-GP1 and membrane phospholipids, as well as between these complexes and heat shock proteins. We also focus into the role of proinflamatory (IL2 / IL6 / TNFalpha) and anti-inflamatory (IL4 / IL-10) cytokines, as well as with the different activation profiles of TCR and/or CD14 (TLR4) and the role of hormones such as melatonin and the growth hormone.

Three to five percent of pregnancies are complicated by preeclampsia (PE). PE is a multisystemic-related endothelial dysfunction disorder characterized by hypertension, proteinuria and renal injury. Despite considerable research, its etiology and pathophysiology still remains unclear. Different theories involving many pathways including thrombophilia, immunologic changes, circulating angiogenic /antiangiogenic factors and increased oxidative stress have been related to its pathogenesis. The role played by antiphospholipid antibodies (aPL) is a matter of discussion in PE.  Biological evidence of endothelial dysfunction related to PE/FGR has been shown by modified plasma markers including fibronectin, von Willebrand factor and ICAM-1 in a similar manner to that which occurs in aPL-related obstetric complications. We are searching now the role played by different aPL and cofactor antibodies, as well as its relationship with angiogenic /antiangiogenic factors and microparticle number in severe PE.