Navegando por Palavras-chave "Fc receptor"

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    Human serum beta(2)-microglobulin levels: correlation with total serum IgG and placental IgG transfer in HIV-infected and non-HIV infected individuals
    (Elsevier B.V., 1999-03-01) Moraes-Pinto, M. I. de; Farhat, C. K.; Fraser, W. D.; Hart, C. A.; Johnson, P. M.; Univ Liverpool; Universidade Federal de São Paulo (UNIFESP)
    The acquisition of maternal immunoglobulin G (IgG) is fundamental to the immune defence of the neonate. the receptor responsible for Ige transfer across the human placenta has also been implicated in the maintenance of IgG levels in the circulation. beta(2)-microglobulin is part of the Fc receptor (FcR) that has recently been purified from the human placenta. in HIV infection, increasing serum levels of total IgG and beta(2)-microglobulin are observed as the disease progresses. Herein: we have investigated the correlation between beta(2)-microglobulin and total serum IgG levels in HIV-seropositive mothers and their term neonates (HIV group, n = 37), as well as in HIV-seronegative mothers and their term neonates (control group, n = 50). Serum maternal beta(2)-microglobulin was directly correlated with total serum IgG levels in HIV-infected mothers (r = 0.58; P = 0.0002), but not in healthy HIV-seronegative mothers (r = - 0.20; P = 0.16). Maternal serum beta(2)-microglobulin was also inversely correlated with placental antibody transfer of total IgG in mother-newborn pairs from the HIV group (r = 0.38; P = 0.02), but not from the control group (r = 0.15, P = 0.31). These results seem to indicate that, in HIV infection, elevated serum beta(2)-microglobulin levels could be involved in maintenance of abnormally high total serum IgG concentrations; by interfering with the binding of IgG to Fc receptors at the maternal-fetal interface, they might also reduce IgG transfer. By contrast, in normal non-HIV infected individuals: serum beta(2)-microglobulin levels do not appear implicated in regulation of these two phenomena. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.
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    Long-term administration of IgG2a anti-NK1.1 monoclonal antibody ameliorates lupus-like disease in NZB/W mice in spite of an early worsening induced by an IgG2a-dependent BAFF/BLyS production
    (Wiley-Blackwell, 2008-10-01) Postol, Edilberto; Meyer, Andre; Cardillo, Fabiola; Alencar, Raquel de; Pessina, Daniel; Nihei, Jorge; Mariano, Mario [UNIFESP]; Mengel, Jose; Fiocruz MS; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    The role of natural killer (NK) T cells in the development of lupus-like disease in mice is still controversial. We treated NZB/W mice with anti-NK1.1 monoclonal antibodies (mAbs) and our results revealed that administration of either an irrelevant immunoglobulin G2a (IgG2a) mAb or an IgG2a anti-NK1.1 mAb increased the production of anti-dsDNA antibodies in young NZB/W mice. However, the continuous administration of an anti-NK1.1 mAb protected aged NZB/W mice from glomerular injury, leading to prolonged survival and stabilization of the proteinuria. Conversely, the administration of the control IgG2a mAb led to an aggravation of the lupus-like disease. Augmented titres of anti-dsDNA in NZB/W mice, upon IgG2a administration, correlated with the production of BAFF/BLyS by dendritic, B and T cells. Treatment with an anti-NK1.1 mAb reduced the levels of interleukin-16, produced by T cells, in spleen cell culture supernatants from aged NZB/W. Adoptive transfer of NK T cells from aged to young NZB/W accelerated the production of anti-dsDNA in recipient NZB/W mice, suggesting that NK T cells from aged NZB/W are endowed with a B-cell helper activity. in vitro studies, using purified NK T cells from aged NZB/W, showed that these cells provided helper B-cell activity for the production of anti-dsDNA. We concluded that NK T cells are involved in the progression of lupus-like disease in mature NZB/W mice and that immunoglobulin of the IgG2a isotype has an enhancing effect on antibody synthesis due to the induction of BAFF/BLyS, and therefore have a deleterious effect in the NZB/W mouse physiology.