Production of auto-anti-idiotype antibody during the normal immune response. XI. Ficoll-induced variations in auto-anti-idiotype production during the response to 2,4,6-trinitrophenyl-Ficoll

The responses to 2,4,6-trinitrophenyl conjugates of different Ficoll preparations differ with respect to the magnitude of the accompanying auto-anti-idiotype (Id) response in both mice and chickens. Evidence is presented that reduced auto-anti-Id production in the chicken is due to the activation of suppressor activity by some preparations of Ficoll.     

Production of auto-anti-idiotypic antibody during the normal immune response: IX. Characteristics of the auto-anti-idiotype antibody and its production

Using hapten-reversible inhibition of plaque formation as an assay for auto-anti-idiotype antibody (anti-Id) and as a means for following idiotype (Id) expression, we have obtained evidence that following immunization with trinitrophenyl (TNP) conjugates (a) there are differences in Id expression in the anti-TNP antibody response to different TNP conjugates although there is some overlap; (b) different strains, although showing some differences in Id expression, tend to produce cross-reactive Ids, thus no obvious allotype linked inheritance of Id expression is observed in this heterogeneous immune response; (c) the auto-anti-Id produced following immunization with TNP-Brucella abortus or TNP-Ficoll tends to be of the IgG_2a and IgG_2b isotypes.     

Production of auto-anti-idiotype antibody during the normal immune response. X. Response to TNP-Ficoll in the chicken

The spontaneous production of auto-anti-idiotype (Id) was demonstrated after injection of chickens with trinitrophenylated Ficoll (TNP-F) by: (a) the presence of hapten-augmentable plaque-forming cells (PFC), (b) the ability of serum and of hapten eluates from immune spleen cells to cause hapten-reversible inhibition of anti-TNP plaque formation, and (c) an enzyme-linked immunosorbent assay (ELISA). Tests for anti-Id using the ELISA and hapten-reversible inhibition of PFC correlated very well. As in the mouse, the incidence of hapten-augmentable PFC was reduced by thymectomy and increased by the transfer of TNP-F-immune spleen cells. Hapten-augmentable PFC were also observed during the immune response of chickens to p-azobenzene arsonate-conjugated Brucella abortus.     

The role of the immune response in helminth population regulation

In natural host-parasite relationships the immune response represents the most effective control against parasitism by those species adapted to life within the environment specified by the host genotype. The parasite population is regulated by immunologically-mediated, often density-dependent, responses which influence establishment, survival and fecundity. The mechanisms underlying such responses have been largely determined by experimental studies using laboratory infections in rodent hosts and are reviewed. The influence of genetic factors which enhance or depress antiparasite immune responses is discussed.     

Role of antigen and,antibody in the regulation of the immune response

The enzyme dextranase could degrade antigenic dextran in vivo even when given 6-15 d after the antigen. Dextranase injected after the antigen suppressed the immune response when given 24 but not 48 h after the antigen, indicating that the antigen must interact with the immune system for 48 h to initiate a response. Thereafter, the B cells are independent of further antigen stimulation. To show whether antibody-mediated suppression of the immune response was determinant specific FITC-conjugated SRC were applied as immunogen and antibodies were raised both against the carrier (SRC) and the FITC hapten. When these antibodies were injected 1-3 h after the immunogen they only suppressed the immune response to the corresponding determinant. Anti-carrier antibodies usually enhanced the response to the hapten. Therefore, antibody-mediated suppression of the immune response is determinant-specific and cannot be mediated in vivo to a detectable extent by the Fc part of the antibodies.     

肠道菌群在机体免疫调节功能中的作用

肠道菌群被称为是人体的一个重要"器官",具有数量庞大、种类繁多等特点,对人体具有重要的生理与病理意义。肠道菌群对机体免疫功能的影响日益受到广泛关注。本文主要就肠道菌群对肠道形态及功能、肠道黏膜免疫系统以及肠道外免疫系统三个方面的影响进行综述。     

高迁移率族蛋白B1的胞外作用与免疫效应

高迁移率族蛋白B1(HMGB1)是一种高度保守的核蛋白,具有调控DNA稳定、复制、转录及翻译等功能.近年来的研究表明,它通过主动或被动的方式被释放至细胞外,并作为一种晚期炎症介质,参与脓毒症等炎症性疾病的发病过程,同时也可作为一种免疫"预警信号"调控机体免疫反应.本文综述了HMGB1的结构、分泌机制、受体信号通路及其对细胞免疫的调控作用.     

Deubiquitylation and regulation of the immune response

Ubiquitylation is a fundamental mechanism of signal transduction that regulates immune responses and many other biological processes. Similar to phosphorylation, ubiquitylation is a reversible process that is counter-regulated by ubiquitylating enzymes and deubiquitylating enzymes (DUBs). Despite the identification of a large number of DUBs, our knowledge of the function and activities of this family of enzymes is just starting to accumulate. As described in this Review, recent studies of several DUBs, in particular CYLD and A20, show that deubiquitylation has an important role in the regulation of both innate and adaptive immune responses.     

The role of the maternal immune system in the regulation of human birthweight

Human birthweight is subject to stabilizing selection. Large babies are at risk of obstetric complications such as obstructed labour, which endangers both mother and child. Small babies are also at risk with reduced survival. Fetal growth requires remodelling of maternal spiral arteries to provide an adequate maternal blood supply to the placenta. This arterial transformation is achieved by placental trophoblast cells, which invade into the uterine wall. Under-invasion is associated with fetal growth restriction; but if invasion is excessive large babies can result. A growing body of evidence suggests that this process is controlled by interactions between killer-cell immunoglobulin-like receptors (KIRs) expressed on maternal uterine natural killer cells (uNK) and their corresponding human leukocyte antigen-C (HLA-C) ligands on invading trophoblast. Mothers with the KIR AA genotype and a fetus with a paternal HLA-C2 allele tend to have small babies, because this combination inhibits cytokine secretion by uNK. Mothers with the activating KIR2DS1 gene and an HLA-C2 fetus are more likely to have large babies. When KIR2DS1 binds to HLA-C2 this increases secretion of cytokines that enhance trophoblast invasion. We conclude that specific combinations of the highly polymorphic gene systems, KIR and HLA-C, contribute to successful reproduction by maintaining birthweight between two extremes.     

The role of lipopolysaccharide-binding protein in modulating the innate immune response

Lipopolysaccharide-binding protein (LBP) has a well-established role in Gram-negative infection. New data suggest a more expanded role for LBP as a general recognition molecule. Several bacterial surface components from Gram-positive pathogens are also recognized by this molecule. LBP may also serve as a clinical marker in severe infections and may carry therapeutic potential.     

Splenic role in the regulation of immune responses.

Evidence for a splenic role in regulating antibody production in other lymphoid tissue was obtained in a system in which cyclical fluctuations of splenic plaque-forming cells (PFC) occur following a single intravenous injection of aggregated human γ-globulin in rabbits. First, PFC arising simultaneously in the mesenteric nodes, peripheral blood, and spleen appear to be derived from the spleen since splenectomy prior to antigen injection abrogated these responses. Second, a noncyclical appearance of PFC in popliteal nodes of rabbits responding to subcutaneous injection of antigen was converted to a cyclical response by simultaneous intravenous injection of antigen, an effect which was abolished by splenectomy prior to antigen injection. It is suggested that, following an intravenous injection of antigen, both suppressor cells as well as antibody-forming precursors may be activated in the spleen and disseminated to other lymphoid tissue.