susceptible mice, bulk splenic T cells were analyzed for expansion, blast formation, and expression of Fas and FasL (Fig 8). T cell expansion was coincident with the generation of parasite specific IgG responses at day fifteen post-infection in resistant mice, but remained near control levels in during the polyclonal B cell activation in susceptible mice at this same time-point. CD69 expression on total T cells was similar early during infection for both models. Later in infection, T cells from infected Balb/c mice experienced a second wave of CD69 activation, which was coincident with clearance of parasite from circulation and the first detection of parasite-specific IgG in circulation, although these levels did increase much until later on during infection (after day 36). Low Fas and FasL expression in Balb/c mice suggests that the contribution of T cells to control of B cell numbers via apoptosis was minimal in these mice. The expression of Fas and FasL on T cells coincided with parasite-specific B cell responses in C57Bl/6 mice, suggesting they may have formed a productive association. Further analysis of T cells at this time-point indicated that resistant mice had significantly higher levels of CD4 and NK T cells than susceptible mice, both of which can provide B cell help . While previous studies show that lack of CD4 T cells led to decreased polyclonal B cell activation , these results suggest that maintenance of CD4 and increased NK T cells may also be important for directing the efficacy of the specific humoral response to parasite antigen. Activation of NK T cells has previously been linked to increased resistance to T. cruzi, but depends upon the presence of CD8 and CD4 T cells, as well as IFN-c production [93,94]. The increased numbers of NK T cells in resistant C57Bl/6 mice is particularly intriguing as they may provide B cell help through direct interaction (CD40L) or rapid cytokine responses, especially IFN-c, which was produced to a much greater extent in these resistant mice . These data provide rationale for further studies to fully define the contribution of CD4 and NK T cells to polyclonal versus parasite-specific humoralimmunity during T. cruzi infection of susceptible versus resistant mice.
In this experiment, the influence of prebiotic and probiotic supplementation in the broiler breeder diets on body w eight, mortality, feed intake, egg production, hatchability and humoralimmunity response w as investigated. A total number of 13140 female and 1260 male breeders (Cobb 500) w ith 26 w ks of age w ere allocated to three treatments w ith six replicates (800 birds each replicate). Breeders w ere fed control basal diet, basal diet supplemented w ith prebiotic (mannan oligosaccharide) or probiotic (Protexin ®) for 17
Our meta-analysis results provide evidence for the involvement of multiple genetic variants (some in LD) within the PVR-PVRL2 gene region (Fig. 1) on chromosome 19 (19q13.31–32) in the genetic control of neutralizing antibody response to rubella vaccine. The poliovirus receptor (PVR, CD155) and poliovirus receptor-related 2 (PVRL2, CD112) genes encode transmembrane glycoproteins/nectins of the immunoglobulin (Ig) superfamily, which are components of adherens junctions and serve as cellular entry receptors for poliovirus (PVR), pseudorabies virus, and certain mutant strains of herpes simplex virus (PRRL2) [17,18,19]. As virus-specific cell surface receptors, these proteins have important functional downstream effects on processes related to viral entry, such as viral replication, cell-to-cell spread, viral tropism, pathogenesis and antiviral immunity. For example, the Ala67Thr mutation in the poliovirus receptor gene (PVR) was previously associated with a higher risk for developing vaccine- induced and wild-type virus-induced poliomyelitis .
Herpes zoster is a viral disease caused by the reactivation of varicella–zoster virus (VZV) which remained latent in the cranial nerve or dorsal root ganglia. Cell-mediated immunity is known to decline with age as part of immunosenescence and can lead to the reactivation of VZV. Whereas herpes zoster is usually mild in healthy young persons, older patients are at increased risk for complications. In the present study we investigated the serum cytokine profile (IL-17, IL-23, IL-21, IL-4, IL-12), representing cellular and humoralimmunity and assessed the level of VZV IgG antibodies in patients with herpes zoster.
ABSTRACT - The objective of this experiment was to evaluate the effect of diet supplementation with vitamins C and E and organic minerals Zn and Se on immunological parameters of broilers from 1 to 35 days, kept on cyclic heat stress (25 to 32°C) and to evaluate the usefulness of bovine serum albumin (BSA) inoculation to determine humoralimmunity. A total of 272 Ross broilers were used to evaluate four types of vitamin-mineral supplementation (VMS): D1- control diet with 60 and 30 IU of vit E for starter and growing diet, respectively, zero vit C, 80 ppm of inorganic Zn, 0.3 ppm of inorganic Se; D2 - control diet + 100 UI vit E and 300 ppm vit C/kg; D3 - control diet + 40 ppm Zn and 0.3 ppm Se/kg, both from organic sources; D4 - control diet and levels of VMS used in D2 and D3), and two environments: thermoneutral (TNA) and cyclic heat stress (CHS) from 14 days of age. Six and five birds per type of supplementation in CHS and TNA, respectively, were inoculated with BSA at 12 and 24 days. Birds serum at 35 days-old was analyzed by ELISA. Supplementation with vitamins and minerals did not influence antibody production of broilers challenged with BSA. Heat stress improved antibody anti-BSA production regardless of the diet. Inoculation with BSA did not influenced broiler performance and was a good strategy to evaluate humoralimmunity of broilers, since the birds responded to the challenge improved antibody production and increased bursal size, despite the higher individual variation.
. Foram realizados dois experimentos alternando a ordem da infecção. Foram avaliados o peso, a eliminação de ovos nas fezes, hemograma, reposta humoral (IgG), análise histopatológica do intestino delgado e morfometria dos granulomas. Foi observado que a cronologia da infecção influenciou os resultados em relação à perda de peso nos grupos coinfectados. Quando o A. ceylanicum antecedeu a infecção por S. mansoni os animais apresentaram a mesma redução de peso, que foi observada no grupo infectado apenas por A. ceylanicum, o que não ocorreu na coinfecção precedida por S. mansoni. Embora A. ceylanicum e S. mansoni sejam hematófagos não houve exacerbação da anemia no grupo coinfectado. O estabelecimento da segunda infecção não foi prejudicado pela infecção prévia, em nenhum dos experimentos realizados, entretanto, houve redução do número de adultos recuperados quando usados na segunda infecção. Não foi observada uma correlação positiva entre a quantidade de ovos de S. mansoni retidos no fígado, ou eliminados nas fezes com a produção de IgG anti- SEA. Em geral no grupo Sm+Acey houve menor produção de IgG. A coinfecção não influenciou a formação, desenvolvimento ou evolução dos granulomas no intestino delgado dos hamsters infectados.
until after completion of the first round of replication in and release from host cells - then no level of pre-existing T cell immunity (i.e., vaccine-induced immunity) will be able to prevent establishment of the infection in a newly infected host or quickly extinguish that infection once it is established. Second, each time T. cruzi invades cells in a “new” site in an infected host (e.g. a site lacking primed effector cells) parasite proliferation would also be expected to proceed there unfettered until the inflamma- tory signals generated by the destruction of the host cell recruit these effector cells beginning four-five days later (upon completion of the replication cycle). Indeed this trend is apparent in the footpad infection assays shown in Fig. 2; for the one and two-time infected/cured mice, as well as early infection in the continuously infected mice, there is essentially no control of parasite load detected in the infection site until after day 4 of infection.
In conclusion, protective immunity against T. cruzi has been well demonstrated in both humans and experi- mental animal models. However, many escape mecha- nisms exist whereby parasites may overcome host pro- tective immunity. While T. cruzi implements some of these mechanisms, it is unable to generate diverse anti- genic lineages or to switch membrane antigens rapidly, which would preclude vaccination. Recent advances toward the development of genetically modified para- sites capable of inducing a protective immune response without causing pathology present a promising new ap-
All organisms are attacked by an ever-changing array of pathogens and parasites, and it is widely supposed that the ensuing host–parasite ‘‘arms race’’ must drive exten- sive adaptive evolution in genes of the immune system. Here we have taken advantage of new sequencing technologies and analytical approaches to quantify the amount of adaptation that is occurring in immunity genes relative to the rest of the genome. We sampled two species of fruit fly (D. melanogaster and D. simulans) from eight different populations around the world, and sequenced 136 immunity and 287 non-immunity genes from these samples. Based on the differences in the sequences between the two species, and the genetic diversity within each species, we have estimated that natural selection drives twice as much change in immune- related proteins as in proteins with no immune function. Interestingly, the rate of adaptation is also more variable among immunity genes than among other genes in the genome, with a small subset of immunity genes evolving under intense natural selection. We suggest that these genes may represent hotspots of host–parasite coevolu- tion within the genome.
Abstract: Tuberculous pleuritis is a good human model to understand the local and protective immune response against tuberculosis, due to the self-limitedness of the disease. Although the cellular immune response has been well characterised in tuberculous pleurisy, much less is known about the humoral immune response operating at the site of infection. To understand the humoral immune response, B cells were enumerated in peripheral blood mononuclear cells (PBMC) and pleural fluid mononuclear cells (PFMC) of tuberculous (TP) and non-tuberculous pleuritis patients (NTP). The levels of IgG, IgA and IgM antibodies for PPD, culture filtrate (CF) and sonicate antigens (Son Ag) were assessed in plasma (BL) and pleural fluid (PF) and a western blot was carried out with the CF antigen. The percentage of CD19 + B-cells was similar in PBMC and PFMC of TP patients but was significantly lower in PFMCs of NTP patients. The IgG levels for PPD and CF antigens were higher in PF of TP than NTP patients. The antigen recognition patterns did not differ in plasma and pleural fluid of the same patient in both groups pointing out the passive diffusion of the plasma to the pleura. The antigens 25, 31, 33, 70, 110, 124 and 132 kDa were recognized exclusively by the TP patients. Thus our study showed that the local humoral response in TP did not differ from the systemic response. However, the humoral response differed in TP patients when compared to NTP patients.
33. McMurray D.N., Loomis S.A.,Casazza L.J., et al. Development of impaired cell-mediated immunity in mild and moderate malnutrition. Am J Clin Nutr 1981;34:68-7. 34. La Grenade L., Schwartz R.A., Janniger C.K. Childhood dermatitis in the tropics: with special emphasis on infective dermatitis, a marker for infection with human T-cell leukemia virus-I. Lancet 1999;353:1951-8. 35. Costa C.M., Goubau P., Liu H.F., et al. HTLV-negative and
Em geral, a saúde e a produtividade de animais alimentados com produtos contaminados com concentrações subletais de citrinina são seriamente prejudicados. A micotoxina modula a resposta inflamatória em aves e mamíferos, interferindo em processos de digestão e secreção de mediadores a partir de células imunocompetentes (Herzog-Soares, 1994; Souza et al., 1997). Uma vez que os componentes do sistema complemento são secretados por fagócitos durante os processos inflamatórios, os efeitos comumente atribuídos às diversas micotoxinas sobre a síntese protéica podem acarretar deficiências na sua produção, permitindo, assim, a permanência de agentes infecciosos e a ocorrência de infecções oportunistas (Corrier, 1991; Freire et al., 1996). Acredita-se que a ação supressiva de micotoxinas sobre a resposta inflamatória tenha efeito bastante significativo sobre a resposta adaptativa humoral em mamíferos diversos (Freire et al., 1996). A citrinina foi caracterizada por não afetar a produção de anticorpos (Reddy et al., 1988; Corrier, 1991), a despeito de causar modificações drásticas nos níveis de leucócitos circulantes, com conseqüente leucopenia (Reddy et al., 1988; Herzog-Soares, 1997). Recentemente, verificou- se que a citrinina também pode estar associada à indução de blastogênese linfocitária (Souza et al., 1999). O objetivo deste trabalho foi determinar o efeito da intoxicação sub-clínica por citrinina sobre a atividade do sistema complemento e sobre a resposta imune humoral para antígenos inertes, durante diferentes fases de imunização, utilizando-se camundongos albinos (Swiss Webstern) como modelo experimental.
Introdução: Sintomas musculoesqueléticos podem representar a primeira manifestação de imunodeficiências humorais primárias. A freqüência de deficiência seletiva de IgA em pacientes com artrite idiopática juvenil (AIJ símile) e lúpus eritematoso sistêmico juvenil (LESJ) é de 2% a 4% e de 1% a 4%, respectivamente. Objetivo: Descrever pacientes que apresentaram artrite como primeiro sinal de uma imunodeficiência humoral primária e determinar a prevalência de deficiência seletiva de IgA em pacientes com diagnóstico de AIJ e LESJ. Pacientes e métodos: Entre janeiro de 1983 e dezembro de 2006, 4.876 pacientes foram acompanhados na Unidade de Reumatologia Pediátrica. Uma avaliação retrospectiva foi realizada em pacientes que apresentaram artrite como primeira manifestação de imunodeficiência. As imunodeficiências humorais foram classificadas em: deficiência seletiva de IgA, hipogamaglobulinemia e deficiência de subclasses de IgG. Resultados: Onze (0,2%) pacientes apresen- taram imunodeficiências humorais: deficiência seletiva de IgA ocorreu em oito, imunodeficiência comum variável em dois e deficiência de subclasses de IgG em um. Cinco dos 11 pacientes apresentaram artrite aguda e seis apresentaram artrite crônica não-erosiva (AIJ símile). Dosagem de imunoglobulinas foi realizada em 70 dos 253 pacientes com AIJ e deficiência seletiva de IgA (IgA sérica < 7 mg/dL) foi de- tectada em 6 (8,5%) – AIJ símile. Dos 45 pacientes com LESJ, com dosagem de IgA realizada, 3 (6,6%) apresentaram deficiência seletiva de IgA. Conclusão: O presente estudo descreveu baixa prevalência de imunodeficiências humorais primárias em pacientes com doenças reumatológicas. Entretanto, a associação entre doenças auto-imunes e imunodeficiências sugere semelhanças em sua etiopatogenia e deve incentivar estudos prospectivos para investigação desta hipótese.
Como a resposta imune humoral envolve a atuação simultânea de uma série de anticorpos que agem em diferentes alvos, uma ACP foi realizada com os dados referentes às respostas de isotipos para as duas proteínas recombinantes, objetivando se avaliar, simultaneamente, os efeitos de todos os anticorpos em uma única análise, uma vez que isso reflete melhor a situação biológica (JAOKO et al., 2007). É importante destacar que, para a inclusão dos dados nesse tipo de análise, tem sido recomendado que eles apresentem distribuição normal (JOLLIFE, 2002). Por essa razão, nós tentamos normalizar os valores de IR referentes às subclasses de anticorpos utilizando a transformação logarítmica. Entretanto, não obtivemos sucesso, o que nos fez optar pelo uso do cálculo , - (WILSON et al., 2008).
HUMORAL RESPONSE OF VACCINATED CATTLE AGAINST TOXINS OF CLOSTRIDIUM BOTULINUM TYPES C AND D AT DIFFERENT AGES. Cattle humoral response against type C and D botulinum toxoids (indirect ELISA) was verified in animals of different ages. The animals (n = 90) were divided in three groups (n = 30): group one (G1): less than two years old; group two (G2): from 2 to 5 years old; group three (G3): more than 5 years old. The groups were vaccinated with two doses [0 and 42 days after primary vaccination (booster)] of bivalent (C and D) antibotulinum vaccine. Group three had higher antibody production (p ≤ 0.05) compared to the other groups, 30 days after the booster. There was no difference (G1 and G2; p ≥ 0.05) in the humoral response against C toxin, however, against D toxin, group one had higher antibody production. It was pos- sible to conclude that after two doses of the commercial bivalent vaccine all groups produced a significant antibody response against botulinum toxins, especially against D type.
Figure 3. Persistence of transgenerational immune priming effects on the increase of immune activity of Manduca sexta offspring after offspring immune challenge by PGN in 21-day-old pupae. A) Increase of phenoloxidase (PO) activity and B) increase of antibacterial (AMP) activity (lysozyme activity equivalent, Micrococcus luteus) were measured in 1-day-old and 3-day-old adults, i.e. three and five days, respectively, after offspring immune treatment in 21-day-old pupae. Female and male parents received a priming treatment in their pupal stage: Naive) untreated, PBS) control-injected with phosphate buffered saline, PGN) injected with peptidoglycan. If the symbol for offspring of naive parents is not visible, it is overlaid by another symbol. Increase of immune activity was measured as increase = (Activity after PGN treatment of the offspring)/ (Mean activity of unchallenged offspring); value 1 is labelled by a line that indicates no change in immune activity after offspring challenge. Please note the comparable scales for increases which show the immunity and visualise the strong priming effects on offspring AMP activity, but the lack of effects on PO activity in the offspring. Mean values 6 SE are given. N = 9 individuals of each developmental stage from each parental group. Means of absolute data of PGN- and PBS-treated offspring are shown in Table S5 in File S1. Differences between the parental priming treatments and the time intervals after offspring PGN treatment were compared by two-way ANOVA (Table 3) and post hoc analysis Tukey tests (Table S7 in File S1). Statistical evaluation of priming effects on the persistence of immunity after offspring immune challenge by PBS is shown in Table S8 in File S1.