**4. Embryotropic antibodies**

Serum content of any "embryotropic" autoantibodies [Poletaev, 2008] in healthy women was restricted by narrow limits (as well as for any other regulatory molecules). But at least in 90% of women suffered from habitual miscarriages, still births, or other forms of pathology of pregnancy, these parameters were changed prominently, and more prominent deviations in autoantibodies accompanied more often and severe reproductive problems [Poletaev & Morozov, 2000; Poletaev et al., 2007]. This phenomenon was successfully used for prognosis of result of planned pregnancy [Poletaev, 2010]. Question is – which of maternal autoantibodies of IgG class should be analyzed first of all (between thousands presented)? In accordance to reproductive function, it seems that abnormal changes in serum content of very different (practically any?) maternal autoantibodies may be causal factors of infertility, miscarriages, or other forms of pregnant pathology. That is to say, that plurality of autoantibodies (with any antigenic specificity) synthesized in mother's organism could be considered as "embryotropic" if they belonged to IgG class. Nor IgМ, nor IgА, or IgE penetrate the placental barrier [Landor, 1995]. However some of them could be more important.

Systemic autoimmune disorders, SLE in particular, are accompanied by prominent rise of infertility and pregnancy losses. The last phenomenon was so typical, that Gleicher as well as Sherer and Shoenfeld have recommended to consider the recurring miscarriages as indication for supposed autoimmune disorder yet undiagnosed in observed woman [Gleicher et al., 1995; Sherer & Shoenfeld, 2004]. Therefore obstetricians can't overlook such a common marker of SLE and other systemic autoimmune disorders as elevated production of autoantibodies against DNA. Lot of publications about negative influences of anti-DNA autoantibodies upon pregnancy development appears yearly. However it is clear now that situation of excess of anti-DNA autoantibodies is no more than particular example of pathogenic immune influences in pregnancy.

Soon after having described antiphospholipid syndrome (APS) as defined nosology form, attention of obstetricians was draw to autoantibodies against phospholipides (cardiolipin, phosphatidilserin, phosphoinisitol, etc.) and against phosplipid-binding serum protein 2- Glycoprotein I; antibodies against the last seemed to be the most informative marker of APS [Sherer & Shoenfeld, 2004; Roubey, 2006]. It should be noted, obstetricians had met APS long before the syndrome was described by G.R.V. Hughes. Because abnormal elevation of anti-cardiolipin autoantibodies was typical for patients with syphilis, and many years was used for diagnostic of syphilis (since 1906: Wasserman' reaction). On other hand, it was known for decades that maternal syphilis was accompanied with rise of still-birth and miscarriage frequency in affected patients [Borisenko et al., 1998].

Fertility is strictly dependent on serum autoantibody level against DNA or cardiolipin, but also depends on changes in autoantibodies against luteinizing hormone, FSH, prolactin [Talwar, 1997], chorionic gonadotropin [Shatavi et al., 2006]. Premature ovarian failure can be accompanied by excessive production of autoantibodies against specific ovarian antigens [Tuohy & Altunas, 2007] and also autoantibodies against chorionic gonadotropin [Shatavi et al., 2006]. Relation to pathology of pregnancy could be associated with autoantibodies against PSG (pregnancy-specific glycoproteins) [Finkenzeller et al., 2000], against Mater (Maternal Antigen that Embryos Require) [Tong et al., 2004; Tuohy et al., 2007], and many others.

birth formation [Poletaev, 2008].

46 From Preconception to Postpartum

Serum content of any "embryotropic" autoantibodies [Poletaev, 2008] in healthy women was restricted by narrow limits (as well as for any other regulatory molecules). But at least in 90% of women suffered from habitual miscarriages, still births, or other forms of pathology of pregnancy, these parameters were changed prominently, and more prominent deviations in autoantibodies accompanied more often and severe reproductive problems [Poletaev & Morozov, 2000; Poletaev et al., 2007]. This phenomenon was successfully used for prognosis of result of planned pregnancy [Poletaev, 2010]. Question is – which of maternal autoantibodies of IgG class should be analyzed first of all (between thousands presented)? In accordance to reproductive function, it seems that abnormal changes in serum content of very different (practically any?) maternal autoantibodies may be causal factors of infertility, miscarriages, or other forms of pregnant pathology. That is to say, that plurality of autoantibodies (with any antigenic specificity) synthesized in mother's organism could be considered as "embryotropic" if they belonged to IgG class. Nor IgМ, nor IgА, or IgE penetrate the placental barrier [Landor, 1995]. However some of them could be more

Systemic autoimmune disorders, SLE in particular, are accompanied by prominent rise of infertility and pregnancy losses. The last phenomenon was so typical, that Gleicher as well as Sherer and Shoenfeld have recommended to consider the recurring miscarriages as indication for supposed autoimmune disorder yet undiagnosed in observed woman [Gleicher et al., 1995; Sherer & Shoenfeld, 2004]. Therefore obstetricians can't overlook such a common marker of SLE and other systemic autoimmune disorders as elevated production of autoantibodies against DNA. Lot of publications about negative influences of anti-DNA autoantibodies upon pregnancy development appears yearly. However it is clear now that situation of excess of anti-DNA autoantibodies is no more than particular example of

Soon after having described antiphospholipid syndrome (APS) as defined nosology form, attention of obstetricians was draw to autoantibodies against phospholipides (cardiolipin, phosphatidilserin, phosphoinisitol, etc.) and against phosplipid-binding serum protein 2- Glycoprotein I; antibodies against the last seemed to be the most informative marker of APS [Sherer & Shoenfeld, 2004; Roubey, 2006]. It should be noted, obstetricians had met APS long before the syndrome was described by G.R.V. Hughes. Because abnormal elevation of anti-cardiolipin autoantibodies was typical for patients with syphilis, and many years was used for diagnostic of syphilis (since 1906: Wasserman' reaction). On other hand, it was known for decades that maternal syphilis was accompanied with rise of still-birth and

Fertility is strictly dependent on serum autoantibody level against DNA or cardiolipin, but also depends on changes in autoantibodies against luteinizing hormone, FSH, prolactin [Talwar, 1997], chorionic gonadotropin [Shatavi et al., 2006]. Premature ovarian failure can be accompanied by excessive production of autoantibodies against specific ovarian antigens [Tuohy & Altunas, 2007] and also autoantibodies against chorionic gonadotropin [Shatavi et al., 2006]. Relation to pathology of pregnancy could be associated with autoantibodies against PSG (pregnancy-specific glycoproteins) [Finkenzeller et al., 2000], against Mater (Maternal

Antigen that Embryos Require) [Tong et al., 2004; Tuohy et al., 2007], and many others.

**4. Embryotropic antibodies** 

pathogenic immune influences in pregnancy.

miscarriage frequency in affected patients [Borisenko et al., 1998].

important.

If we will take in mind that autoantibodies are biologically active regulatory molecules it will be evident, not only excessive production, but also shortages in many (any?)
