Recent studies provide some evidence for the contribution of antibody-mediated autoimmune mechanisms to the nature of fibromyalgia (FM) and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Much attention was paid to the autoantibodies (AAb) targeting G protein-coupled receptors as natural components of the immune system. However, the natural AAb network is much more extensive, and has not been previously investigated in these disorders. The enzyme immunoassays ELI-Viscero-Test and ELI-Neuro-Test were used to determine changes in serum content of 33 natural AAb to neural, organ-specific and non-tissue-specific autoantigens (a) in 11 ME/CFS patients with comorbid FM; (b) in 11 ME/CFS patients without FM; (c) in 11 healthy controls. Individual AAb profiles and their correlation with some clinical symptoms were analyzed. Both patients with ME/CFS(−)FM and ME/CFS(+)FM were characterized by more frequent and pronounced deviations in the immunoreactivity to GABA-receptors than healthy controls. Although the level of other natural AAb did not differ between study groups, AAb correlation signatures were altered in patients compared to healthy controls. Both in patients and healthy controls the level of natural AAb to various neural and tissue-specific antigens correlated with the severity of fatigue, bodily pain, depression, anxiety, physical and mental health-related quality of life. Notably, widely different correlation patterns were observed between study groups. Findings from this pilot study provide some evidence that the homeostasis of autoimmune relationships, which are possibly a physiological part of our immune system, may be altered in FM and ME/CFS. The correlation of disease-induced perturbations in individual AAb profiles with some clinical symptoms may arise from the immune system’s ability to reflect qualitative and quantitative changes in antigenic composition of the body.

Autism is a vexed problem today. Overall, there is a high frequency of birth children (1:80 -1:150) with late diagnosed autism spectrum disorders (ASD) and this trend is getting progressively stronger. The causes for the currently increased frequency of ASD and the pathogenesis of ASD are not fully understood yet. One of the most likely mechanisms inducing ASD may be a maternal immune imprinting. This phenomenon is based on transplacental translocation of maternal antibodies of IgG class and, as a consequence, on the epigenetic "tuning" of immune system of the fetus and child. This mechanism provides development of child's anti-infection resistance before meeting with microorganisms, but it can be also a cause of inborn pathology including the ASD appearance. The quantitative changes in maternal blood serum autoantibodies depend on a specifi c microbial population, or are induced by environmental chemical pollutants in association with some individual features of the maternal metabolism. These immune changes are adaptive in most cases for the maternal organism, but can be pathogenic for the fetus in some cases. We discuss in the present paper the possibilities to predict the risk from abnormal development of nervous system in fetus and early diagnosis of ASD in high-risk group of children. : autism, diagnosis, ASD, CNS pathology, immune imprinting, autoantibodies, cytokines Folia Medica 2014; 56(2): 73-80 Copyright © 2014 Medical University, Plovdiv РЕЗЮМЕ Частота случаев рождения детей, страдающих расстройствами аутистического спектра (РАС) с каждым годом растет и сегодня составляет 1:80 -1:150 в глобальном масштабе. Причины этого, как и "собственно" патогенез РАС, остаются не вполне понятными. Одним из наиболее вероятных механизмов, запускающих формирование РАС, во многих случаях, является феномен материнского иммунного импринтинга, основанный на трансплацентарном поступлении антител матери класса IgG к плоду и эпигенетической «настройке» иммунной системы будущего ребенка. Иммунный импринтинг обеспечивает формирование противоинфекционной резистентности у ребенка еще во внутриутробном периоде (до встречи с инфектами), но, в некоторых случаях, он может быть причиной ряда нарушений и, в частности, формирования РАС. Особенности репертуаров аутоантител (а-АТ) матери могут зависеть от превалирования у нее тех или иных бактериально-вирусных ассоциатов, а также от индивидуальных особенностей организма женщины. Соответствующие иммунные изменения как правило являются адаптивными для матери, однако, для будущего ребенка могут являться патогенными. Обсуждаются возможности прогнозирования риска развития плода и новорожденного с патологией нервной системы у женщин с аномалиями репертуаров а-АТ, а также ранней диагностики РАС у детей группы риска, начиная с первых месяцев жизни. Ключевые слова : аутизм, диагностика, РАС, патология ЦНС, иммунный импринтинг, аутоантитела, цитокины Folia Medica 2014; 56(2): 73-80 Keywords