Maternal immune response to pregnancy

Abstract

The pregnant female is exposed to a variety of potentially immunogenic foreign antigens on her allogenic intra-uterine conceptus. The extent to which maternal antibodies and cell-mediated immune responses to these antigens are relevant to the paradoxical survival of the fetal allograft is not clearly established. The key to the maintenance of pregnancy lies in the trophoblast. This tissue prevents significant entry of maternal lymphocytes to the fetus and is most likely to protected from maternal immune rejection by features of its cell surface molecular structure and/or its synthesis of factors that render it insusceptible to antibody- or cell-mediated immune lysis in vivo. An alternative, or complementary, protective system, involving maternal recognition and immunoregulatory processes that deviate responses away from the expected rejection reactions, may also operate but has not yet been convincingly demonstrated. Such a mechanism is unlikely to involve the classically defined histocompatibility classically defined histocompatibility antigen system, at least in human pregnancy, where there is an absence of Class I antigens from the trophoblast but increasing evidence of trophoblast-associated antigens and related immune responses. It remains to be established whether unexplained recurrent miscarriage in women and spontaneous abortion in animal models is caused by failure of maternal immunoregulatory control or by non-immunological factors. This is relevant to the validity of immunotherapeutic approaches to the prevention of early fetal loss.

Replicative homeostasis II: Influence of polymerase fidelity on RNA virus quasispecies biology: Implications for immune recognition, viral autoimmunity and other "virus receptor" diseases

“…For many classical autoimmune disorders, including primary biliary cirrhosis [59], multiple sclerosis, and rheumatoid arthritis, convincing epidemiological evidence [60], including cases clustering [61,62], strongly suggests these diseases are triggered by infectious agents in genetically predisposed individuals. In others, such as diabetes mellitus, tantalizing epidemiological [63], clinical [64] and laboratory [65] evidence has implicated enteroviruses, but has suggested viral-triggered autoimmune processes, rather than cytolytic destruction of pancreatic betacells [66].…”

“…Is it possible that self-limiting infections like influenza and SARS also autoregulate their replication, and, like HCV or HBV, become partially dormant, yet remain transcriptionally active, in the face of an active and powerful immune response? PCR amplification of influenza RNA from convalescent samples makes this readily testable, while the documented relationship of influenza to myocardial infarction [132] and juvenile rheumatoid arthritis [61] makes the question important. If confirmed, the well-documented seasonality of some depressive illnesses [158] and schizophrenia, [146] and increased rates of schizophrenia during influenza epidemics [144], and the increased incidence of both depression [146] and schizophrenia [144,145] following in-utero exposure to influenza may be more rationally explained.…”

Immunology of the cutaneous disorders of pregnancy

“…albuminuria, thus making the differential diagnosis from pre-eclampsia very difficult. [56][57][58] As PV is mediated by antibodies, it exacerbates during gestation, and the IgG antibodies that are able to cross the Among the most frequent complications of SLE during pregnancy are abortion, premature delivery, fetal death, placenta can produce cutaneous transitory skin lesions in the neonate. The use of systemic steroids rather than hypertensive disease of pregnancy, retarded intrauterine growth, and neonatal lupus.…”

“…70 are present in 10-20% of patients with SLE, and they are associated with abortion, thrombosis, thrombocytopenia, Urticarial dermatoses with hormonal influence A group of urticarial dermatoses related or unrelated to and hemolytic anemia. [56][57][58][59][60] The activity of SLE can be correlated with the incidence pregnancy has been described. Estrogenic dermatitis with urticarial flare ups associated with the menstrual cycle of exacerbation of the disease.…”

À procura do Ped bovino

“…As células trofoblásticas do córion são as únicas células fetais em contato direto com o epitélio uterino e o sistema imune materno(DAVIES, et al, 2000). Por este motivo, o TF é a barreira anatômica responsável pela sobrevivência do feto não alogênico ou semi-alogênico em desenvolvimento(BILLINGTON, 1989).A prenhez pode ser considerada como um balanço imunológico no qual o sistema imune da mãe deve se tornar tolerante aos antígenos paternos do MHC presentes no feto e ainda manter normal sua competência imune para se defender contra microorganismos(WEETMAN, 1999). Na maioria dos mamíferos a proteção do feto parece envolver o bloqueio da expressão de antígenos polimórficos do MHC nas células trofoblásticas que recobrem a porção externa da placenta, bem como a manutenção de um estado de quiescência imunológica ou imunossupressão do útero.…”